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1.
Medicine (Baltimore) ; 99(6): e18926, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-32028400

RESUMO

Lymphoid follicles/aggregates in gastric biopsies have been traditionally linked to Helicobacter pylori gastritis, and less commonly to other inflammatory and neoplastic conditions. The frequency of such aggregates in normal stomachs has yet to be adequately evaluated. This is especially relevant when it comes to diagnosing non-specific chronic gastritis in biopsy specimens with chronic inflammation but no evidence of H pylori infection. Sleeve gastrectomies represent an opportunity to study adequately preserved gastric mucosa in patients who are otherwise asymptomatic and lack a history of gastric disease.To study sleeve gastrectomy specimens to quantify the amount of lymphoid follicles/aggregates and lymphocytic infiltration in normal stomachs.Sixty-eight bariatric sleeve gastrectomies and 13 control specimens from Whipple resections were examined for multiple histologic features including type, quantity, and distribution of chronic inflammation and lymphoid follicles/aggregates. Presence of H pylori was documented by both Hematoxylin and eosin-stained (H&E) and immunohistochemistry (IHC). Clinical information including age, sex, medication intake, prior endoscopy, and/or H pylori infection was recorded. The patient population was divided in 2 groups, H pylori negative versus H pylori positive, and statistical analysis was performed by a biostatistician.Two hundred sixty three fundic sections from 68 bariatric patients were examined. Fifty three patients were found to be H pylori-negative, compared with 15 who were positive for H pylori. Among the H pylori-negative group, the average number of lymphoid aggregates was 3.33, compared with an average of 6.26 in the H pylori positive group (the difference was statistically significant with a P-value of .008). The average number of plasma cells per high power field was 2.15 in the H pylori negative group, compared and average of 5.07 in the H pylori positive group (the difference was also statistically significant with a P-value <.001). Clinically, 10 of the 53 H pylori-negative patients had esophagogastroduodenoscopy (EGD) that showed endoscopic mild non-erosive gastric erythema. The remaining had no documentation of symptoms or medication intake, including Non-steroidal anti-inflammatory drugs (NSAIDs) and Proton Pump Inhibitors (PPI).Our results suggest that the presence of lymphoid aggregates and plasma cells infiltration can be a normal finding in otherwise normal gastric mucosa, though more pronounced in H pylori infected patients.


Assuntos
Mucosa Gástrica/patologia , Gastrite/patologia , Infecções por Helicobacter/patologia , Helicobacter pylori/isolamento & purificação , Tecido Linfoide/citologia , Plasmócitos/citologia , Estudos de Casos e Controles , Feminino , Gastrectomia , Gastrite/diagnóstico , Humanos , Masculino
2.
APMIS ; 128(1): 25-34, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31628820

RESUMO

Eradication failure of Helicobacter pylori infection could play a causal role in progression of gastric disorders. In this study, infection with H. pylori was followed in gastric biopsies of symptomatic adult patients at two phases during 1-year period. Analyses were done to show association of therapeutic regimens with the refractory infection, changes in sequence types (STs) and minimum inhibitory concentration (MIC) values, and progression of histopathological changes. Infection with H. pylori was confirmed in 32.3% (57/170) of the patients. Persistent infection with H. pylori was confirmed in 14 out of the 25 patients (56%) who participated at the second phase of the study. A difference between primary and secondary resistance rates to clarithromycin (49% vs 64.3%), metronidazole (76.36% vs 100%), and ciprofloxacin (45% vs 57.1%) was detected. Although the re-emerged strains in patients with refractory infection did not show alteration in STs, their MIC50 values showed twofold increases for clarithromycin and ciprofloxacin. While ciprofloxacin containing regimens were more successful, failure of metronidazole containing regimens was detected in 77% of the patients. Consequently, inappropriate medication has an impact on refractory H. pylori infection, which could cause to a rise in resistance levels to antibiotics and progression of pathological disorders.


Assuntos
Antibacterianos/uso terapêutico , Farmacorresistência Bacteriana Múltipla , Infecções por Helicobacter/tratamento farmacológico , Infecções por Helicobacter/patologia , Helicobacter pylori/efeitos dos fármacos , Idoso , Idoso de 80 Anos ou mais , Antibacterianos/farmacologia , Técnicas de Tipagem Bacteriana , Biópsia , Ciprofloxacino/farmacologia , Claritromicina/farmacologia , Feminino , Seguimentos , Técnicas Histológicas , Humanos , Concentração Inibidora 50 , Masculino , Testes de Sensibilidade Microbiana , Pessoa de Meia-Idade , Tipagem de Sequências Multilocus , Estômago/microbiologia , Estômago/patologia
3.
Arq Gastroenterol ; 56(4): 419-424, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31800739

RESUMO

BACKGROUND: Helicobacter pylori infection is the most important risk factor for gastric atrophy and intestinal metaplasia, both considered gastric cancer precursor lesions. Therefore, the investigation of the occurrence of H. pylori infection, precursor lesions and associated factors guides the adoption of specific strategies for the control this type of cancer. OBJECTIVE: To evaluate the prevalence of H. pylori infection in patients undergoing upper digestive endoscopy, as well as the prevalence of intestinal metaplasia, atrophy and chronic inflammation and their association with H. pylori infection. METHODS: A retrospective study was performed based on reports of gastric endoscopic biopsies performed in a private laboratory affiliated to the Brazilian Public Health System (SUS). Patients were evaluated for age, gender and type of health service. The samples were evaluated for the presence of H. pylori, and also of chronic inflammation, intestinal metaplasia and glandular atrophy. RESULTS: Of a total of 4,604 patients (mean age 51±16.6), 63.9% were female and 63.1% coming from private health care service. The prevalence of H. pylori infection was 31.7% (n=1,459), and the percentage of infection was significantly higher in patients from public health service (42.0%) in relation to patients from private health service (25.6%). Among H. pylori (+) patients, a higher percentage of intestinal metaplasia (17.7% vs 13.3%) and glandular atrophy (17.6% vs 6.9%) were observed when compared to those H. pylori (-) (P<0.01). From the patients H. pylori (+) with at least one type of precursor lesion (n=418), 161 (38.5%) had metaplasia and chronic inflammation, 160 (38.3%) had atrophy and chronic inflammation and finally 97 (23.2%) presented metaplasia, atrophy and chronic inflammation simultaneously. CONCLUSION: The present study reinforces the association of H. pylori infection with gastric cancer precursor lesions in a Brazilian population, emphasizing the importance of infection prevention measures, as well as the treatment of infected patients, especially in regions with lower socioeconomic levels that show a higher prevalence of infection by H. pylori.


Assuntos
Infecções por Helicobacter/patologia , Helicobacter pylori , Neoplasias Gástricas/microbiologia , Adulto , Idoso , Atrofia/microbiologia , Biópsia , Doença Crônica , Feminino , Gastroscopia , Humanos , Masculino , Metaplasia/microbiologia , Pessoa de Meia-Idade , Lesões Pré-Cancerosas/microbiologia , Prevalência , Estudos Retrospectivos , Fatores de Risco , Neoplasias Gástricas/patologia
4.
Arq Bras Cir Dig ; 32(4): e1480, 2019.
Artigo em Inglês, Português | MEDLINE | ID: mdl-31859933

RESUMO

BACKGROUND: The presence of intestinal metaplasia in the distal esophagus (Barrett's esophagus) is an important precursor of adenocarcinoma. Knowledge of the risk factors and the process by which the Barrett develops is very important and Helicobacter pylori (HP) can contribute to this development. AIM: To analyze the impact of HP in the gastric mucosa with intestinal metaplasia in the distal esophagus in areas of columnar epithelialization smaller than 10 mm in length and epidemiological data on prevalence. METHOD: A retrospective study in which were included 373 consecutive patients diagnosed with columnar epithelium in the distal esophagus was done. In all, HP was investigated by urease and histology, exclusion and inclusion factors were applied and patients were divided into two groups: the first grouping the ones without histological diagnosis of Barrett's esophagus (235-63%) and the second with it (138-37%). RESULTS: There was no significant difference between HP and non-HP patients in relation to the probability of having intestinal metaplasia (p=0.587). When related to the general group, there was an inverse association between the bacterium and the columnar epithelia in the distal esophagus. Age (p=0.031), gender (p=0.013) and HP (p=0.613) when related together to intestinal metaplasia showed no significant relation. In isolation, when related to age and gender, regardless of HP, results confirmed that patients in more advanced age and women present a higher incidence of intestinal metaplasia. CONCLUSION: There is an inverse relation between HP and the areas of columnar epithelization in the distal esophagus, regardless of the presence or absence of intestinal metaplasia. Age and gender, regardless of HP, showed higher prevalence in women and in older the number of cases with intestinal metaplasia in the distal esophagus.


Assuntos
Esôfago de Barrett/patologia , Epitélio/patologia , Infecções por Helicobacter/patologia , Helicobacter pylori , Adulto , Fatores Etários , Idoso , Esôfago de Barrett/microbiologia , Epitélio/microbiologia , Feminino , Humanos , Masculino , Metaplasia/microbiologia , Metaplasia/patologia , Pessoa de Meia-Idade , Estudos Retrospectivos , Fatores Sexuais
5.
PLoS Genet ; 15(11): e1008497, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31747390

RESUMO

The lipopolysaccharide O-antigen structure expressed by the European Helicobacter pylori model strain G27 encompasses a trisaccharide, an intervening glucan-heptan and distal Lewis antigens that promote immune escape. However, several gaps still remain in the corresponding biosynthetic pathway. Here, systematic mutagenesis of glycosyltransferase genes in G27 combined with lipopolysaccharide structural analysis, uncovered HP0102 as the trisaccharide fucosyltransferase, HP1283 as the heptan transferase, and HP1578 as the GlcNAc transferase that initiates the synthesis of Lewis antigens onto the heptan motif. Comparative genomic analysis of G27 lipopolysaccharide biosynthetic genes in strains of different ethnic origin revealed that East-Asian strains lack the HP1283/HP1578 genes but contain an additional copy of HP1105 and JHP0562. Further correlation of different lipopolysaccharide structures with corresponding gene contents led us to propose that the second copy of HP1105 and the JHP0562 may function as the GlcNAc and Gal transferase, respectively, to initiate synthesis of the Lewis antigen onto the Glc-Trio-Core in East-Asian strains lacking the HP1283/HP1578 genes. In view of the high gastric cancer rate in East Asia, the absence of the HP1283/HP1578 genes in East-Asian H. pylori strains warrants future studies addressing the role of the lipopolysaccharide heptan in pathogenesis.


Assuntos
Infecções por Helicobacter/genética , Lipopolissacarídeos/genética , Antígenos O/genética , Neoplasias Gástricas/genética , Grupo com Ancestrais do Continente Asiático , Fucosiltransferases/genética , Fucosiltransferases/imunologia , Glucanos/genética , Glicosiltransferases/genética , Glicosiltransferases/imunologia , Infecções por Helicobacter/imunologia , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/patologia , Helicobacter pylori/genética , Helicobacter pylori/imunologia , Helicobacter pylori/patogenicidade , Humanos , /imunologia , Lipopolissacarídeos/química , Lipopolissacarídeos/imunologia , Mutagênese , Antígenos O/imunologia , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/imunologia , Neoplasias Gástricas/patologia
6.
World J Gastroenterol ; 25(39): 6025-6040, 2019 Oct 21.
Artigo em Inglês | MEDLINE | ID: mdl-31660038

RESUMO

BACKGROUND: Allicin (2-propene-1-sulfinothioic acid S-2-propenyl ester, diallyl thiosulfinate) extracted from garlic, has proven activity against Helicobacter pylori (H. Pylori) infection. In recent years, clinical trials have explored its utility as an add-on therapy with variable outcomes reported. AIM: To perform a systemic review of allicin as an add-on treatment for H. Pylori infection and assess its efficacy in randomized controlled trials (RCTs). METHODS: Electronic databases including MEDLINE, EMBASE, the Web of Science, the Cochrane Database, the China National Knowledge Infrastructure Database, Chinese VIP Information Databases, Chinese Medical Databases, and the Wan-Fang Database were searched for keywords including "allicin", "Helicobacter pylori", "randomized clinical trials", and their synonyms. A meta-analysis was performed using the fixed-effects model for low heterogeneity and the random-effects model for high heterogeneity with sensitivity analysis. Bias was evaluated using Egger's tests. Trial sequential analysis (TSA) was used to evaluate information size and treatment benefits. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) was used to assess the level of quality, and studies were classed as "high quality", "moderate quality", "low quality", and "very low quality". RESULTS: A total of eight RCTs consisting of 867 participants (435 from the allicin group and 432 from the control group) were included. Eradication rate in the allicin group (93.33%, 406/435) was significantly higher than that of the control group (83.56%, 361/432) [I 2 = 0%, odds ratio (OR) = 2.75, 95% confidence interval (CI): 1.74-4.35, P < 0.001]. The healing rate of ulcers following H. pylori therapy in the allicin group (86.17%, 349/405) was significantly higher than that of the control group (75.87%, 305/402) [I 2 = 0%, OR = 2.05, 95%CI: 1.39-3.03, P < 0.001]. The total remission rate of peptic ulcers across all allicin groups was 97.16%, which was significantly higher than that of controls [96.05% (389/405) vs 86.55% (360/402), I 2 = 0, OR = 3.04, 95%CI: 1.51-6.12, P = 0.015]. No significant differences in side effects were observed. TSA suggested that the trials were of sufficient standard to draw reliable conclusions. The quality of outcomes including eradication rates and side effects was graded as "very low" due to downgrades for "risk of bias" and "indirectness". Other outcomes such as ulcer healing rates and total ulcer remission rates were graded as "low" due to downgrades for "risk of bias". CONCLUSION: Allicin as an add-on therapy improves H. pylori eradication, healing of ulcers, and remission of symptoms. These results are suggested to be treated with caution due to limited quality.


Assuntos
Anti-Infecciosos/administração & dosagem , Infecções por Helicobacter/tratamento farmacológico , Úlcera Gástrica/tratamento farmacológico , Ácidos Sulfínicos/administração & dosagem , Antiácidos/administração & dosagem , Antiácidos/efeitos adversos , Antibacterianos/administração & dosagem , Antibacterianos/efeitos adversos , Anti-Infecciosos/efeitos adversos , Ensaios Clínicos como Assunto , Quimioterapia Combinada/efeitos adversos , Quimioterapia Combinada/métodos , Mucosa Gástrica/efeitos dos fármacos , Mucosa Gástrica/microbiologia , Mucosa Gástrica/patologia , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/patologia , Helicobacter pylori/efeitos dos fármacos , Helicobacter pylori/isolamento & purificação , Humanos , Inibidores da Bomba de Prótons/administração & dosagem , Inibidores da Bomba de Prótons/efeitos adversos , Indução de Remissão/métodos , Úlcera Gástrica/microbiologia , Úlcera Gástrica/patologia , Ácidos Sulfínicos/efeitos adversos , Resultado do Tratamento
7.
PLoS Pathog ; 15(9): e1007921, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31568537

RESUMO

Humans are frequently exposed to bacterial genotoxins involved in digestive cancers, colibactin and Cytolethal Distending Toxin (CDT), the latter being secreted by many pathogenic bacteria. Our aim was to evaluate the effects induced by these genotoxins on nuclear remodeling in the context of cell survival. Helicobacter infected mice, coculture experiments with CDT- and colibactin-secreting bacteria and hepatic, intestinal and gastric cells, and xenograft mouse-derived models were used to assess the nuclear remodeling in vitro and in vivo. Our results showed that CDT and colibactin induced-nuclear remodeling can be associated with the formation of deep cytoplasmic invaginations in the nucleus of giant cells. These structures, observed both in vivo and in vitro, correspond to nucleoplasmic reticulum (NR). The core of the NR was found to concentrate ribosomes, proteins involved in mRNA translation, polyadenylated RNA and the main components of the complex mCRD involved in mRNA turnover. These structures are active sites of mRNA translation, correlated with a high degree of ploidy, and involve MAPK and calcium signaling. Additional data showed that insulation and concentration of these adaptive ribonucleoprotein particles within the nucleus are dynamic, transient and protect the cell until the genotoxic stress is relieved. Bacterial genotoxins-induced NR would be a privileged gateway for selected mRNA to be preferably transported therein for local translation. These findings offer new insights into the context of NR formation, a common feature of many cancers, which not only appears in response to therapies-induced DNA damage but also earlier in response to genotoxic bacteria.


Assuntos
Toxinas Bacterianas/toxicidade , Helicobacter/patogenicidade , Ribonucleoproteínas/metabolismo , Animais , Linhagem Celular , Núcleo Celular/efeitos dos fármacos , Núcleo Celular/metabolismo , Núcleo Celular/patologia , Sobrevivência Celular , Dano ao DNA , Infecções por Helicobacter/metabolismo , Infecções por Helicobacter/patologia , Hepatócitos/metabolismo , Hepatócitos/patologia , Humanos , Camundongos , Camundongos Endogâmicos C57BL , Microscopia Eletrônica de Transmissão , Mutagênicos/toxicidade , Peptídeos/toxicidade , Policetídeos/toxicidade , RNA Mensageiro/metabolismo
8.
BMJ ; 366: l5016, 2019 Sep 11.
Artigo em Inglês | MEDLINE | ID: mdl-31511230

RESUMO

OBJECTIVE: To assess the effects of Helicobacter pylori treatment, vitamin supplementation, and garlic supplementation in the prevention of gastric cancer. DESIGN: Blinded randomized placebo controlled trial. SETTING: Linqu County, Shandong province, China. PARTICIPANTS: 3365 residents of a high risk region for gastric cancer. 2258 participants seropositive for antibodies to H pylori were randomly assigned to H pylori treatment, vitamin supplementation, garlic supplementation, or their placebos in a 2×2×2 factorial design, and 1107 H pylori seronegative participants were randomly assigned to vitamin supplementation, garlic supplementation, or their placebos in a 2×2 factorial design. INTERVENTIONS: H pylori treatment with amoxicillin and omeprazole for two weeks; vitamin (C, E, and selenium) and garlic (extract and oil) supplementation for 7.3 years (1995-2003). MAIN OUTCOME MEASURES: Primary outcomes were cumulative incidence of gastric cancer identified through scheduled gastroscopies and active clinical follow-up through 2017, and deaths due to gastric cancer ascertained from death certificates and hospital records. Secondary outcomes were associations with other cause specific deaths, including cancers or cardiovascular disease. RESULTS: 151 incident cases of gastric cancer and 94 deaths from gastric cancer were identified during 1995-2017. A protective effect of H pylori treatment on gastric cancer incidence persisted 22 years post-intervention (odds ratio 0.48, 95% confidence interval 0.32 to 0.71). Incidence decreased significantly with vitamin supplementation but not with garlic supplementation (0.64, 0.46 to 0.91 and 0.81, 0.57 to 1.13, respectively). All three interventions showed significant reductions in gastric cancer mortality: fully adjusted hazard ratio for H pylori treatment was 0.62 (95% confidence interval 0.39 to 0.99), for vitamin supplementation was 0.48 (0.31 to 0.75), and for garlic supplementation was 0.66 (0.43 to 1.00). Effects of H pylori treatment on both gastric cancer incidence and mortality and of vitamin supplementation on gastric cancer mortality appeared early, but the effects of vitamin supplementation on gastric cancer incidence and of garlic supplementation only appeared later. No statistically significant associations were found between interventions and other cancers or cardiovascular disease. CONCLUSIONS: H pylori treatment for two weeks and vitamin or garlic supplementation for seven years were associated with a statistically significant reduced risk of death due to gastric cancer for more than 22 years. H pylori treatment and vitamin supplementation were also associated with a statistically significantly reduced incidence of gastric cancer. TRIAL REGISTRATION: ClinicalTrials.gov NCT00339768.


Assuntos
Infecções por Helicobacter/terapia , Lesões Pré-Cancerosas/terapia , Neoplasias Gástricas/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Antiulcerosos/administração & dosagem , Biópsia , China/epidemiologia , Suplementos Nutricionais , Quimioterapia Combinada/métodos , Feminino , Seguimentos , Alho/química , Mucosa Gástrica/microbiologia , Mucosa Gástrica/patologia , Gastroscopia , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/patologia , Helicobacter pylori/isolamento & purificação , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Extratos Vegetais/administração & dosagem , Lesões Pré-Cancerosas/microbiologia , Lesões Pré-Cancerosas/patologia , Inibidores da Bomba de Prótons/administração & dosagem , Neoplasias Gástricas/patologia , Neoplasias Gástricas/prevenção & controle , Análise de Sobrevida , Taxa de Sobrevida , Fatores de Tempo , Resultado do Tratamento , Vitaminas/administração & dosagem
9.
World J Gastroenterol ; 25(33): 4870-4884, 2019 Sep 07.
Artigo em Inglês | MEDLINE | ID: mdl-31543679

RESUMO

Helicobacter pylori (H. pylori) is one of the most important human pathogens, infecting approximately half of the global population. Despite its high prevalence, only a subset of H. pylori infected individuals develop serious gastroduodenal pathology. The pathogenesis of H. pylori infection and disease outcome is thus thought to be mediated by an intricate interplay between host, environmental and bacterial virulence factors. H. pylori has adapted to the harsh milieu of the human stomach through possession of various virulence genes that enable survival of the bacteria in the acidic environment, movement towards the gastric epithelium, and attachment to gastric epithelial cells. These virulence factors enable successful colonization of the gastric mucosa and sustain persistent H. pylori infection, causing chronic inflammation and tissue damage, which may eventually lead to the development of peptic ulcers and gastric cancer. Numerous studies have focused on the prevalence and role of putative H. pylori virulence genes in disease pathogenesis. While several virulence factors with various functions have been identified, disease associations appear to be less evident, especially among different study populations. This review presents key findings on the most important H. pylori virulence genes, including several bacterial adhesins and toxins, in children and adults, and focuses on their prevalence, clinical significance and potential relationships.


Assuntos
Mucosa Gástrica/microbiologia , Infecções por Helicobacter/microbiologia , Helicobacter pylori/patogenicidade , Fatores de Virulência/genética , Virulência/genética , Adesinas Bacterianas/genética , Mucosa Gástrica/patologia , Genes Bacterianos , Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/patologia , Helicobacter pylori/genética , Humanos , Prevalência
10.
World J Gastroenterol ; 25(35): 5220-5232, 2019 Sep 21.
Artigo em Inglês | MEDLINE | ID: mdl-31558869

RESUMO

Helicobacter pylori (H. pylori) is a Gram-negative bacterium with a number of virulence factors, such as cytotoxin-associated gene A, vacuolating cytotoxin A, its pathogenicity island, and lipopolysaccharide, which cause gastrointestinal diseases. Connexins function in gap junctional homeostasis, and their downregulation is closely related to gastric carcinogenesis. Investigations into H. pylori infection and the fine-tuning of connexins in cells or tissues have been reported in previous studies. Therefore, in this review, the potential mechanisms of H. pylori-induced gastric cancer through connexins are summarized in detail.


Assuntos
Carcinogênese/patologia , Conexinas/metabolismo , Infecções por Helicobacter/patologia , Helicobacter pylori/patogenicidade , Neoplasias Gástricas/patologia , Regulação para Baixo , Mucosa Gástrica/patologia , Regulação Neoplásica da Expressão Gênica , Ilhas Genômicas , Infecções por Helicobacter/microbiologia , Helicobacter pylori/genética , Helicobacter pylori/metabolismo , Interações Hospedeiro-Patógeno , Humanos , Neoplasias Gástricas/microbiologia , Fatores de Virulência/genética , Fatores de Virulência/metabolismo
11.
Helicobacter ; 24 Suppl 1: e12645, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31486233

RESUMO

This article is a review of the most important, accessible, and relevant literature published between April 2018 and April 2019 in the field of Helicobacter species other than Helicobacter pylori. The initial part of the review covers new insights regarding the presence of gastric and enterohepatic non-H. pylori Helicobacter species (NHPH) in humans and animals, while the subsequent section focuses on the progress in our understanding of the pathogenicity and evolution of these species. Over the last year, relatively few cases of gastric NHPH infections in humans were published, with most NHPH infections being attributed to enterohepatic Helicobacters. A novel species, designated "Helicobacter caesarodunensis," was isolated from the blood of a febrile patient and numerous cases of human Helicobacter cinaedi infections underlined this species as a true emerging pathogen. With regard to NHPH in animals, canine/feline gastric NHPH cause little or no harm in their natural host; however they can become opportunistic when translocated to the hepatobiliary tract. The role of enterohepatic Helicobacter species in colorectal tumors in pets has also been highlighted. Several studies in rodent models have further elucidated the mechanisms underlying the development of NHPH-related disease, and the extra-gastric effects of a Helicobacter suis infection on brain homeostasis was also studied. Comparative genomics facilitated a breakthrough in the evolutionary history of Helicobacter in general and NHPH in particular. Investigation of the genome of Helicobacter apodemus revealed particular traits with regard to its virulence factors. A range of compounds including mulberries, dietary fiber, ginseng, and avian eggs which target the gut microbiota have also been shown to affect Helicobacter growth, with a potential therapeutic utilization and increase in survival.


Assuntos
Gastroenteropatias/epidemiologia , Gastroenteropatias/microbiologia , Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/microbiologia , Helicobacter/classificação , Helicobacter/isolamento & purificação , Doenças dos Animais/epidemiologia , Doenças dos Animais/microbiologia , Doenças dos Animais/patologia , Animais , Gastroenteropatias/patologia , Gastroenteropatias/veterinária , Helicobacter/genética , Helicobacter/patogenicidade , Infecções por Helicobacter/patologia , Infecções por Helicobacter/veterinária , Humanos , Meningites Bacterianas/epidemiologia , Meningites Bacterianas/microbiologia , Meningites Bacterianas/patologia , Sepse/epidemiologia , Sepse/microbiologia , Sepse/patologia
12.
Helicobacter ; 24 Suppl 1: e12638, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31486234

RESUMO

In this review, we shall focus on the last year progression understanding the pathogenesis of Helicobacter pylori infection in the light of recent data related to adaptation of H pylori to the harsh acidic environment in the stomach, colonization of gastric mucosa via interaction with mucin 5 (MUC5AC) and other host cell receptors, the ability to form biofilm, interference with the host metabolic pathways, and induction of neuroimmune cross-talk as well as downregulation of gastric barrier homeostasis and its consequences for the disease development. The role of the membrane vesicles of these bacteria has been emphasized as an important source of virulence factors. Furthermore, we shall describe molecular and functional studies on new aspects of VacA and CagA virulence, including the role of urease in the upregulation of VacA toxicity, an epithelial-mesenchymal transition mediated by CagA, and the role of interaction of HopQ adhesin with carcinoembryonic antigen-related cell adhesion molecules (CEACAMs) in CagA translocation into the host cells by the type IV secretion system (T4SS). The role of molecular mimicry between a common sequence (ATVLA) of H pylori heat shock protein (Hsp) B and human Hsp60 in the induction of potentially autoreactive antibodies is discussed. All these new data illustrate further progress in understanding H pylori pathogenicity and facilitate the search for new therapeutic targets as well as development of immunoprophylaxis methods based on new chimeric UreB and HpA proteins.


Assuntos
Células Epiteliais/microbiologia , Células Epiteliais/patologia , Infecções por Helicobacter/patologia , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori/patogenicidade , Interações Hospedeiro-Patógeno , Humanos , Fatores Imunológicos/metabolismo , Fatores de Virulência/metabolismo
13.
Helicobacter ; 24 Suppl 1: e12644, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31486236

RESUMO

Chronic inflammation induced by Helicobacter pylori infection is a critical factor in the development of peptic ulcer disease and gastric cancer. Central to this inflammation is the initiation of pro-inflammatory signaling cascades within epithelial cells, in particular those mediated by two sensors of bacterial cell wall components, nucleotide-binding oligomerization domain-containing protein 1 (NOD1) and alpha-protein kinase 1 (ALPK1). H pylori is, however, also highly adept at mitigating inflammation in the host, thereby restricting tissue damage and favoring bacterial persistence. H pylori modulates host immune responses by altering cytokine signaling in epithelial and myeloid cells, which results in increased proliferation of regulatory T cells and downregulation of effector T-cell responses. H pylori vacuolating cytotoxin A (VacA) has been shown to play an important role in the dampening of immune responses and induction of immune tolerance capable of protecting against asthma. It is also possible to generate protective immune responses by immunization with various H pylori antigens or their epitopes, in combination with an adjuvant, though this for now has only been shown in mouse models. Novel non-toxic adjuvants, consisting of modified bacterial enterotoxins or nanoparticles, have recently been developed that may not only enhance vaccine efficacy, but also help translate candidate vaccines to the clinic. This review will summarize the main discoveries in the past year regarding host immune responses to H pylori infection, as well as the design of new vaccine approaches against this infection.


Assuntos
Vacinas Bacterianas/imunologia , Infecções por Helicobacter/imunologia , Infecções por Helicobacter/patologia , Helicobacter pylori/imunologia , Helicobacter pylori/patogenicidade , Interações Hospedeiro-Patógeno , Vacinas Bacterianas/isolamento & purificação , Pesquisa Biomédica/tendências , Células Epiteliais/imunologia , Células Epiteliais/microbiologia , Infecções por Helicobacter/prevenção & controle , Humanos , Tolerância Imunológica , Inflamação/imunologia , Inflamação/patologia , Inflamação/prevenção & controle , Células Mieloides/imunologia , Células Mieloides/microbiologia , Linfócitos T Reguladores/imunologia
14.
Helicobacter ; 24 Suppl 1: e12637, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31486237

RESUMO

This review covers recent publications investigating the relationship between Helicobacter pylori infection and gastroesophageal reflux disease, Barrett's esophagus, eosinophilic esophagitis, peptic ulcer disease (PUD), H pylori gastritis, and functional dyspepsia. In the area of gastroesophageal reflux disease, new data suggest that reflux may have a role in the transmission of H pylori infection. In addition to several observational studies, data on alterations in esophageal physiology in patients with H pylori infection are presented. Further evidence for the inverse relationship between H pylori infection and Barrett's esophagus is available in the form of a meta-analysis from the North American Barrett's and Esophageal Carcinoma Consortium. The relationship between H pylori infection and eosinophilic esophagitis remains uncertain. Although new data do not indicate a significantly lower prevalence of H pylori among patients with eosinophilic esophagitis, a meta-analysis showed a 37% reduced risk of eosinophilic esophagitis among H pylori-infected patients. Novel data are presented on the genetic variability of bacterial virulence factors and their relationship with PUD. We also report data on plasma biomarkers, which may detect progression to gastric cancer in H pylori-associated PUD. A new meta-analysis was published, which assessed the risk of PUD in low-dose aspirin users with H pylori infection. Finally, we report on the ongoing attempts to stratify patients with gastritis using endoscopic methods when compared to standard biopsy examination.


Assuntos
Gastroenteropatias/etiologia , Gastroenteropatias/patologia , Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/patologia , Helicobacter pylori/isolamento & purificação , Humanos , Prevalência
15.
Helicobacter ; 24 Suppl 1: e12636, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31486239

RESUMO

In the last year, many studies have demonstrated a potential role of Helicobacter pylori in the pathogenic mechanisms of different extragastric diseases. While the role of H pylori in idiopathic thrombocytopenic purpura, idiopathic iron deficiency anemia, and vitamin B12 deficiency has already been demonstrated, there is growing evidence of other related conditions, especially cardiovascular, metabolic, and neurologic disorders, including neurodegenerative diseases. A summary of the results of the most relevant studies published over the last year on this attractive topic is presented in this review.


Assuntos
Doenças Cardiovasculares/etiologia , Infecções por Helicobacter/patologia , Helicobacter pylori/isolamento & purificação , Doenças Metabólicas/etiologia , Doenças do Sistema Nervoso/etiologia , Doenças Cardiovasculares/patologia , Humanos , Doenças Metabólicas/patologia , Doenças do Sistema Nervoso/patologia
16.
Int J Mol Sci ; 20(15)2019 Jul 31.
Artigo em Inglês | MEDLINE | ID: mdl-31370155

RESUMO

Despite the significant recent advances in clinical practice, gastric cancer (GC) represents a leading cause of cancer-related deaths in the world. In fact, occurrence of chemo-resistance still remains a daunting hindrance to effectiveness of the current approach to GC therapy. There is accumulating evidence that a plethora of cellular and molecular factors is implicated in drug-induced phenotypical switching of GC cells. Among them, epithelial-mesenchymal transition (EMT), autophagy, drug detoxification, DNA damage response and drug target alterations, have been reported as major determinants. Intriguingly, resistant GC phenotype may be the result of GC cell-induced tumor microenvironment (TME) remodeling, which is currently emerging as a key player in promoting drug resistance and overcoming cytotoxic effects of drugs. In this review, we discuss the possible mechanisms of drug resistance and their involvement in determining current GC therapies failure.


Assuntos
Autofagia/genética , Resistencia a Medicamentos Antineoplásicos/genética , Regulação Neoplásica da Expressão Gênica , Neovascularização Patológica/genética , Neoplasias Gástricas/genética , Microambiente Tumoral/genética , Transportadores de Cassetes de Ligação de ATP/genética , Transportadores de Cassetes de Ligação de ATP/metabolismo , Antineoplásicos/uso terapêutico , Autofagia/efeitos dos fármacos , Proteínas Relacionadas à Autofagia/genética , Proteínas Relacionadas à Autofagia/metabolismo , Sobrevivência Celular/genética , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Células Epiteliais/patologia , Transição Epitelial-Mesenquimal/genética , Infecções por Helicobacter/tratamento farmacológico , Infecções por Helicobacter/genética , Infecções por Helicobacter/metabolismo , Infecções por Helicobacter/patologia , Helicobacter pylori/crescimento & desenvolvimento , Helicobacter pylori/patogenicidade , Humanos , Hipóxia/tratamento farmacológico , Hipóxia/genética , Hipóxia/metabolismo , Hipóxia/patologia , Inativação Metabólica/genética , MicroRNAs/genética , MicroRNAs/metabolismo , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/metabolismo , Neovascularização Patológica/tratamento farmacológico , Neovascularização Patológica/metabolismo , Neovascularização Patológica/patologia , Neoplasias Gástricas/tratamento farmacológico , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Microambiente Tumoral/efeitos dos fármacos
17.
Nutrients ; 11(8)2019 Aug 12.
Artigo em Inglês | MEDLINE | ID: mdl-31409000

RESUMO

Helicobacter pylori (H. pylori) may be involved in diabetes and other insulin-related processes. This study aimed to investigate the associations between H. pylori infection and the risks of type 2 diabetes, impaired glucose tolerance (IGT), diabetic nephropathy, and poor glycemic control. We retrospectively evaluated 16,091 subjects without diabetes at baseline who underwent repeated health examinations. Subjects were categorized according to whether they were seropositive and seronegative for H. pylori infection. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazard models. The serological results were validated using an independent cohort (n = 42,351) based on a histological diagnosis of H. pylori infection. During 108,614 person-years of follow-up, 1338 subjects (8.3%) developed newly diagnosed diabetes, although the cumulative incidence of diabetes was not significantly related to serological H. pylori status. The multivariate Cox proportional-hazards regression models revealed that H. pylori seropositivity was not significantly associated with diabetes (HR: 1.01, 95% CI: 0.88-1.16; p = 0.854), IGT (HR: 0.98, 95% CI: 0.93-1.04; p = 0.566), diabetic nephropathy (HR: 0.99, 95% CI: 0.82-1.21; p = 0.952), or poor glycemic control (HR: 1.05, 95% CI: 0.90-1.22; p = 0.535). Similarly, histopathological findings of H. pylori infection were not significantly associated with diabetes (p = 0.311), diabetic nephropathy (p = 0.888), or poor glycemic control (p = 0.989). The findings from these large Korean cohorts indicate that there does not appear to be a role for past H. pylori infection in the development of diabetes, IGT, diabetic nephropathy, or poor glycemic control.


Assuntos
Diabetes Mellitus Tipo 2 , Infecções por Helicobacter , Helicobacter pylori/crescimento & desenvolvimento , Glicemia/metabolismo , Estudos de Casos e Controles , Diabetes Mellitus Tipo 2/sangue , Diabetes Mellitus Tipo 2/etiologia , Diabetes Mellitus Tipo 2/microbiologia , Nefropatias Diabéticas/etiologia , Feminino , Intolerância à Glucose/etiologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/patologia , Humanos , Hiperglicemia/etiologia , Masculino , Pessoa de Meia-Idade , Modelos de Riscos Proporcionais , República da Coreia , Estudos Retrospectivos , Fatores de Risco
18.
World J Gastroenterol ; 25(30): 4105-4124, 2019 Aug 14.
Artigo em Inglês | MEDLINE | ID: mdl-31435167

RESUMO

Gastric cancer remains the third leading cause of mortality from cancer worldwide and carries a poor prognosis, due largely to late diagnosis. The importance of the interaction between Helicobacter pylori (H. pylori) infection, the main risk factor, and host-related genetic factors has been studied intensively in recent years. The genetic predisposition for non-hereditary gastric cancer is difficult to assess, as neither the real prevalence of premalignant gastric lesions in various populations nor the environmental risk factors for cancer progression are clearly defined. For non-cardiac intestinal-type cancer, identifying the factors that modulate the progression from inflammation toward cancer is crucial in order to develop preventive strategies. The role of cytokines and their gene variants has been questioned in regard to non-self-limiting H. pylori gastritis and its evolution to gastric atrophy and intestinal metaplasia; the literature now includes various and non-conclusive results on this topic. The influence of the majority of cytokine single nucleotide polymorphisms has been investigated for gastric cancer but not for preneoplastic gastric lesions. Among the investigated gene variants onlyIL10T-819C, IL-8-251, IL-18RAP917997, IL-22 rs1179251, IL1-B-511, IL1-B-3954, IL4R-398 and IL1RN were identified as predictors for premalignant gastric lesions risk. One of the most important limiting factors is the inhomogeneity of the studies (e.g., the lack of data on concomitant H. pylori infection, methods used to assess preneoplastic lesions, and source population). Testing the modifying effect of H. pylori infection upon the relationship between cytokine gene variants and premalignant gastric lesions, or even testing the interaction between H. pylori and cytokine gene variants in multivariable models adjusted for potential covariates, could increase generalizability of results.


Assuntos
Citocinas/genética , Mucosa Gástrica/patologia , Infecções por Helicobacter/epidemiologia , Lesões Pré-Cancerosas/patologia , Neoplasias Gástricas/patologia , Atrofia/epidemiologia , Atrofia/etiologia , Atrofia/patologia , Progressão da Doença , Mucosa Gástrica/microbiologia , Predisposição Genética para Doença , Infecções por Helicobacter/patologia , Helicobacter pylori/isolamento & purificação , Humanos , Metaplasia/epidemiologia , Metaplasia/etiologia , Metaplasia/patologia , Polimorfismo de Nucleotídeo Único , Lesões Pré-Cancerosas/epidemiologia , Lesões Pré-Cancerosas/etiologia , Fatores de Risco , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/etiologia
19.
Helicobacter ; 24(5): e12653, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31411795

RESUMO

BACKGROUND: Colonization of the gastric mucosa with Helicobacter pylori (Hp) leads to the cascade of pathologic events including local inflammation, gastric ulceration, and adenocarcinoma formation. Paracrine loops between tissue cells and Hp contribute to the formation of gastric cancerous loci; however, the specific mechanisms underlying existence of these loops remain unknown. We determined the phenotypic properties of gastric fibroblasts exposed to Hp (cagA+vacA+) infection and their influence on normal epithelial RGM-1 cells. MATERIALS AND METHODS: RGM-1 cells were cultured in the media conditioned with Hp-activated gastric fibroblasts. Their morphology and phenotypical changes associated with epithelial-mesenchymal transition (EMT) were assessed by Nomarski and fluorescence microscopy and Western blot analysis. Motility pattern of RGM-1 cells was examined by time-lapse video microscopy and transwell migration assay. The content of TGF-ß in Hp-activated fibroblast-conditioned media was determined by ELISA. RESULTS: The supernatant from Hp-activated gastric fibroblasts caused the EMT-like phenotypic diversification of RGM-1 cells. The formation of fibroblastoid cell sub-populations, the disappearance of their collective migration, an increase in transmigration potential with downregulation of E-cadherin and upregulation of N-cadherin proteins, prominent stress fibers, and decreased proliferation were observed. The fibroblast (CAF)-like transition was manifested by increased secretome TGF-ß level, α-SMA protein expression, and its incorporation into stress fibers, and the TGF-ßR1 kinase inhibitor reduced the rise in Snail, Twist, and E-cadherin mRNA and increased E-cadherin expression induced by CAFs. CONCLUSION: Gastric fibroblasts which are one of the main targets for Hp infection contribute to the paracrine interactions between Hp, gastric fibroblasts, and epithelial cells. TGF-ß secreted by Hp-activated gastric fibroblasts prompting their differentiation toward CAF-like phenotype promotes the EMT-related phenotypic shifts in normal gastric epithelial cell populations. This mechanism may serve as the prerequisite for GC development.


Assuntos
Células Epiteliais/patologia , Transição Epitelial-Mesenquimal , Fibroblastos/patologia , Infecções por Helicobacter/patologia , Fator de Crescimento Transformador beta/metabolismo , Animais , Células Cultivadas , Helicobacter pylori/crescimento & desenvolvimento , Interações Hospedeiro-Patógeno , Modelos Teóricos , Ratos Sprague-Dawley
20.
Helicobacter ; 24(5): e12655, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31411799

RESUMO

BACKGROUND: Various studies reported the relationship between Helicobacter pylori (H pylori) and vitamin D, but there is some controversy around that. This study aimed to conduct a meta-analysis to clarify the relationship between vitamin D and H pylori infection, and vitamin D and H pylori eradication. METHODS: Articles published until June 1, 2019, in the PubMed, MEDLINE, and EMBASE databases with English-language medical studies were searched. According to the inclusion criteria, relevant statistical data were extracted to Microsoft Excel and analyzed by STATA15.1. RESULTS: Ten articles were finally included. It was demonstrated that average 25(OH)D level in H pylori-positive patients was lower than H pylori-negative (SMD = -0.53 ng/mL, 95% CI = (-0.91, -0.16 ng/mL)). For H pylori eradication individuals, the result showed that average 25(OH)D level in H pylori successful eradication individuals was higher than unsuccessful (SMD = 1.31 ng/mL, 95% CI = [0.60, 2.02 ng/mL]). In addition, individuals with vitamin D deficiency had lower H pylori eradicate rate (OR = 0.09, 95% CI = [0.02, 0.41]). Sensitivity analysis showed that the meta-analysis results were stable and reliable. CONCLUSIONS: Vitamin D was a protective factor to H pylori infection. Moreover, vitamin D can improve the success rate of H pylori eradication.


Assuntos
Infecções por Helicobacter/tratamento farmacológico , Infecções por Helicobacter/patologia , Deficiência de Vitamina D/complicações , Vitamina D/sangue , Quimioterapia Combinada/métodos , Humanos , Sensibilidade e Especificidade , Resultado do Tratamento
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