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1.
PLoS One ; 15(9): e0238944, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32966303

RESUMO

BACKGROUND AND AIMS: Patients that have failed therapy for Helicobacter pylori (H. pylori) infection are incompletely characterized. The aim of this study was to characterize a H. pylori treatment resistant cohort compared to the cohorts of newly diagnosed, earlier eradicated and non-infected. MATERIAL AND METHODS: Patients were selected from routine referrals to the Endoscopy units at three different Norwegian hospitals. In all four cohorts, gastric biopsies were scored according to the Sydney classification, and symptoms according to the Gastrointestinal Symptom Rating Scale score, including sub-scores for upper gastrointestinal symptoms and functional bowel symptoms. Patients in the H. pylori resistant group were treated with a triple therapy regimen that consisted of levofloxacin, amoxicillin and a proton pump inhibitor. RESULTS: We included 185 patients, 42 H. pylori treatment resistant, 50 newly diagnosed, 61 previously H. pylori eradicated and 32 never infected. The treatment-resistant cohort had higher scores for upper gastrointestinal symptoms and functional bowel symptoms compared to the other groups except for the group being never H. pylori infected. The H. pylori resistant patients had lower Sydney scores than patients with newly diagnosed H. pylori infection. The triple combination showed a high efficacy of 91% to eradicate H. pylori. CONCLUSIONS: Patients with treatment-resistant H. pylori infection had more gastrointestinal symptoms, but a lower Sydney score than patients with newly diagnosed infection. A treatment regimen including levofloxacin showed a high efficacy in eradicating H. pylori in patients that previously had failed eradication treatment.


Assuntos
Farmacorresistência Bacteriana/efeitos dos fármacos , Infecções por Helicobacter/tratamento farmacológico , Helicobacter pylori/efeitos dos fármacos , Idoso , Amoxicilina/uso terapêutico , Antibacterianos/farmacologia , Quimioterapia Combinada , Feminino , Infecções por Helicobacter/metabolismo , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori/metabolismo , Helicobacter pylori/patogenicidade , Humanos , Levofloxacino/uso terapêutico , Masculino , Pessoa de Meia-Idade , Inibidores da Bomba de Prótons/uso terapêutico
2.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi ; 35(8): 744-749, 2019 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-31638572

RESUMO

Objective To demonstrate HpaA can intensify the inflammatory response and gastric mucosa injury by IL-21 from induced T cell. Methods Biopsy specimens were taken from gastric mucosa of 56 patients with H.pylori infection before and after H.pylori radical elimination by endoscope. The levels of IL-21, matrix metalloproteinase-2 (MMP2) and MMP9 from the biopsy were detected by reverse transcription PCR and Western blot analysis. Meanwhile, the recombinant HpaA was cloned, expressed and purified to stimulate the magnetic cell sorting CD3+ T cells from healthy donors' peripheral blood mononuclear cells (PBMCs), and the level of IL-21 in the supernatant fluid was detected by ELISA. Thereafter, AGS cells were cultured and Western blot analysis was performed to detect the levels of MMP2 and MMP9 in the AGS cells with human IL-21 and anti-IL-21 antibody treatment for 24 hours. Results The protein levels of IL-21 and MMP2 and MMP9 in gastric mucosa infected with H. pylori was significantly higher than that in gastric mucosa after radical treatment of H. pylori. Meanwhile, the recombinant HpaA promoted IL-21 secretion by induced CD3+T cells in vitro. IL-21 stimulated the expression of MMP2 and MMP9 in AGS cells. When IL-21 was blocked by the antibody, the levels of MMP2 and MMP9 in AGS cells decreased significantly. Conclusion HpaA plays a significant role in the gastric mucosa injury caused by H.pylori infection through IL-21 from induced T cells.


Assuntos
Adesinas Bacterianas , Mucosa Gástrica , Interleucinas , Linfócitos T , Adesinas Bacterianas/metabolismo , Mucosa Gástrica/lesões , Mucosa Gástrica/fisiopatologia , Infecções por Helicobacter/imunologia , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori/imunologia , Helicobacter pylori/metabolismo , Humanos , Interleucinas/metabolismo , Leucócitos Mononucleares/imunologia , Leucócitos Mononucleares/metabolismo , Linfócitos T/metabolismo
3.
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
4.
PLoS One ; 14(8): e0221643, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31465466

RESUMO

BACKGROUND: Chronic systemic inflammation is an important causative factor in the pathogenesis of atherosclerosis. However, the effect of chronic Helicobacter pylori (Hp) infection on arterial stiffness, a predictor of cardiovascular events, remains unclear. We evaluated the association between Hp infection and arterial stiffness in asymptomatic healthy individuals. METHODS: Arterial stiffness was evaluated using the cardio-ankle vascular index (CAVI). We included subjects who underwent CAVI and anti-Hp IgG antibody evaluations, simultaneously, between March 2013 and July 2017. Demographic characteristics and metabolic and cardiovascular parameters were compared with respect to anti-Hp IgG antibody status. Multivariable logistic regression analyses were performed to determine the effect of Hp-seropositivity and conventional cardiovascular risk factors on arterial stiffness. RESULTS: Of 2,251 subjects, 1,326 (58.9%) were included in the Hp-seropositive group. Median age (P < 0.001) and systolic blood pressure (P = 0.027) were significantly higher in the Hp-seropositive than in the Hp-seronegative group. Levels of LDL-cholesterol were significantly higher in the Hp-seropositive than in the Hp-seronegative group (P = 0.016). Other serum metabolic parameters were not significantly different between the two groups. The median CAVI value and the proportion of subjects with a CAVI ≥ 8 were significantly higher in the Hp-seropositive than in the Hp-seronegative group (both P < 0.001). On multivariable logistic regression analyses, Hp-seropositivity, age, body mass index, waist circumference, smoking, hypertension, diabetes mellitus, and dyslipidemia were significantly associated with high CAVI values. In the subgroup analysis conducted according to age group, a tendency towards an increased association between Hp-seropositivity and CAVI was observed with increasing age, even though the difference did not reach the statistical significance. CONCLUSIONS: Hp-seropositivity was significantly associated with arterial stiffness. Hp infection may contribute to the development of cardiovascular diseases.


Assuntos
Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/fisiopatologia , Rigidez Vascular , Fatores Etários , Anticorpos Antibacterianos/sangue , Anticorpos Antibacterianos/imunologia , Biomarcadores , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/fisiopatologia , Estudos Transversais , Suscetibilidade a Doenças , Feminino , Infecções por Helicobacter/complicações , Infecções por Helicobacter/microbiologia , Helicobacter pylori/imunologia , Humanos , Masculino , Pessoa de Meia-Idade , Prevalência , Vigilância em Saúde Pública , Fatores de Risco , Estudos Soroepidemiológicos
5.
Mol Biol Rep ; 46(6): 5703-5712, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31359381

RESUMO

Helicobacter pylori (H. pylori) has been shown to be one of the leading causes of peptic ulcer diseases (PUDs) and gastritis. T helper-22 (Th22) cells and its most important cytokine, interleukin-22 (IL-22) are importantly active in inflammation and inflammatory tissues. Since inflammation is one of the main attributes of infection caused by H. pylori and resulting complications (gastritis and gastrointestinal ulcer), this study was designed to evaluate the Th22 cells count and the IL-22 protein expression in people suffering from PUD and gastritis. The present study was conducted on 55 patients with gastritis, 47 patients with PUD and 48 uninfected subjects. After preparation of section and extraction of protein from antral biopsies, immunohistochemistry and western blot methods were used to evaluate the Th22 cells and IL-22 protein expression level, respectively. According to findings, the Th22 cells count and the IL-22 protein expression level in the infected subjects were siginficantly more than in the uninfected subjects. It should be noted that the Th22 cells count and the IL-22 protein expression level in the infected subjects with PUD were significantly greater than those in the infected subjects with gastritis. In addition, the Th22 cells count had positive correlation with the density of H. pylori, chronic inflammation score and acute inflammatory score in the infected subjects with PUD. The Th22 cells count had positive correlation with the Th17 cells count and inverse correlation with the Treg cells count in the infected subjects with PUD and gastritis. Our data demonstrated that abnormal hyper-activation of Th22 cells as well as its correlation with the Th17 cells during infection caused by H. pylori might damage tissues through immunopathological responses.


Assuntos
Gastrite/imunologia , Infecções por Helicobacter/imunologia , Interleucinas/imunologia , Úlcera Péptica/imunologia , Linfócitos T Auxiliares-Indutores/imunologia , Adulto , Idoso , Feminino , Mucosa Gástrica/química , Mucosa Gástrica/imunologia , Mucosa Gástrica/metabolismo , Mucosa Gástrica/patologia , Gastrite/fisiopatologia , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori , Humanos , Inflamação/imunologia , Inflamação/fisiopatologia , Interleucinas/metabolismo , Masculino , Pessoa de Meia-Idade , Úlcera Péptica/fisiopatologia , Antro Pilórico/química , Antro Pilórico/imunologia , Antro Pilórico/metabolismo , Antro Pilórico/patologia , Estudos Retrospectivos , Índice de Gravidade de Doença , Linfócitos T Auxiliares-Indutores/metabolismo
6.
Isr Med Assoc J ; 5(21): 339-344, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-31140227

RESUMO

BACKGROUND: The prevalence of Helicobacter pylori varies geographically by age, race, and socioeconomic status (SES). However, the impact of ethnicity on endoscopic outcomes in infected individuals is not well known. OBJECTIVES: To assess the impact of ethnicity among Israelis with biopsy-proven H. pylori infection. METHODS: A retrospective study, including patients who underwent gastroscopy and were diagnosed histologically with H. pylori infection, was conducted. Information on demographics, SES, medications, and co-morbidities were extracted from medical records. Univariate (Student's t-test, chi-square test) and multivariate (multinomial and logistic) regression analysis were conducted to examine the predictors of the clinical outcome. RESULTS: The study included 100 Israeli Jews and 100 Israeli Arabs diagnosed with biopsy-proven H. pylori infection. At univariate analysis, the number of households was higher among Arabs (P < 0.001), whose family income and parental education were lower than among Jews (P < 0.001 for both variables). The response to amoxicillin and clarithromycin differed between the two groups, being higher among Jews (P < 0.001).In clinical outcomes (gastritis severity, gastric and duodenal ulcer, intestinal metaplasia, atrophic gastritis, and MALT), no statistically significant differences could be detected between Jews and Arabs. Concerning intestinal metaplasia, lack of consumption of nonsteroidal anti-inflammatory drugs resulted a statistically significant protective factor (odds ratio 0.128, 95% confidence interval 0.024-0.685, P = 0.016). CONCLUSIONS: Although in the literature ethnicity seems to be a risk factor for H. pylori colonization, no statistical significance was detected in various endoscopic and histological findings related to H. Pylori infection between Israeli Arabs and Jews.


Assuntos
Amoxicilina/uso terapêutico , Claritromicina/uso terapêutico , Mucosa Gástrica , Gastrite , Gastroscopia , Infecções por Helicobacter , Helicobacter pylori/isolamento & purificação , Adulto , Antibacterianos/uso terapêutico , Árabes/estatística & dados numéricos , Biópsia/métodos , Biópsia/estatística & dados numéricos , Demografia , Feminino , Mucosa Gástrica/microbiologia , Mucosa Gástrica/patologia , Gastrite/etnologia , Gastrite/patologia , Gastrite/fisiopatologia , Gastroscopia/métodos , Gastroscopia/estatística & dados numéricos , Infecções por Helicobacter/tratamento farmacológico , Infecções por Helicobacter/etnologia , Infecções por Helicobacter/patologia , Infecções por Helicobacter/fisiopatologia , Humanos , Israel/epidemiologia , Judeus/estatística & dados numéricos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Fatores Socioeconômicos
7.
Anal Cell Pathol (Amst) ; 2019: 9506863, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31093484

RESUMO

This study was undertaken to further investigate the CD177 expression in Helicobacter pylori- (Hp-) infected wild-type and CD177-/- C57BL/6 mice, which may be helpful to elucidate the relationship between CD177 and Hp-related gastritis. 20 WT mice were randomly assigned into the Hpss1 WT group (n = 10) and Hp49503 WT group (n = 10); 20 KO mice were randomly assigned into the Hpss1 KO group (n = 10) and Hp49503 KO group (n = 10). The remaining mice served as controls. Mice in the HpSS1 groups and Hp49503 groups were independently infected with corresponding strains. Results showed that the Hp colonization score was related to the grade of mucosal inflammation (P < 0.05). The inflammation grade was comparable between the HpSS1 group and Hp49503 group as well as between the WT group and KO group. In addition, the Hp colonization score was related to the CD177 expression score (P < 0.05). The CD177 expression in the Hp colonization group was higher than that in the non-Hp colonization group (P < 0.05). CD177 expression was positively related to the inflammation grade (P < 0.01). In conclusion, CD177 expression was similar between HP49503- and HPss1-infected WT C57BL/6 mice, and CD177 expression was undetectable in CD177-/- mice. CD177 expression in the gastric mucosa increases with the elevation of inflammation grade. In Hp-infected mice, the inflammation grade had no relationship with the type of Hp strain and the CD177 expression, but the mucosal inflammation score in Hp-infected mice was higher than that in non-Hp infected mice.


Assuntos
Antígenos CD/metabolismo , Proteínas Ligadas por GPI/metabolismo , Gastrite/metabolismo , Infecções por Helicobacter/metabolismo , Helicobacter pylori , Isoantígenos/metabolismo , Receptores de Superfície Celular/metabolismo , Animais , Mucosa Gástrica/metabolismo , Mucosa Gástrica/microbiologia , Mucosa Gástrica/fisiopatologia , Gastrite/microbiologia , Infecções por Helicobacter/fisiopatologia , Humanos , Camundongos , Camundongos Endogâmicos C57BL
8.
Int J Mol Sci ; 20(8)2019 Apr 18.
Artigo em Inglês | MEDLINE | ID: mdl-31003453

RESUMO

BACKGROUND: Helicobacter pylori (H. pylori) eradication therapy may improve gastric atrophy and intestinal metaplasia, but the results of previous studies have not always been consistent. The aim of this study was to compare the histological changes of intestinal metaplasia and gastric atrophy among the use of acid-suppressing drugs after H. pylori eradication. METHODS: A cohort of 242 patients who underwent successful eradication therapy for H. pylori gastritis and surveillance endoscopy examination from 1996 to 2015 was analyzed. Changes in the histological scores of intestinal metaplasia and atrophy according to drug use (proton-pump inhibitors (PPIs), H2 receptor antagonists (H2RAs), and non-acid suppressant use) were evaluated in biopsies of the antrum and corpus using a generalized linear mixed model in all patients. RESULTS: The mean follow-up period and number of biopsies were 5.48 ± 4.69 years and 2.62 ± 1.67 times, respectively. Improvement in the atrophy scores of both the antrum (p = 0.042) and corpus (p = 0.020) were significantly superior in patients with non-acid suppressant drug use compared with those of PPI and H2RA use. Metaplasia scores in both the antrum and corpus did not improve in all groups, and no significant differences were observed among groups in the antrum (p = 0.271) and corpus (p = 0.077). CONCLUSIONS: Prolonged acid suppression by PPIs or H2RAs may limit the recovery of gastric atrophy following H. pylori eradication.


Assuntos
Atrofia/tratamento farmacológico , Infecções por Helicobacter/tratamento farmacológico , Helicobacter pylori/efeitos dos fármacos , Inibidores da Bomba de Prótons/administração & dosagem , Adulto , Idoso , Idoso de 80 Anos ou mais , Atrofia/microbiologia , Atrofia/fisiopatologia , Atrofia/prevenção & controle , Endoscopia , Feminino , Ácido Gástrico/metabolismo , Mucosa Gástrica/efeitos dos fármacos , Mucosa Gástrica/microbiologia , Mucosa Gástrica/fisiopatologia , Gastrite/tratamento farmacológico , Gastrite/microbiologia , Gastrite/fisiopatologia , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori/metabolismo , Helicobacter pylori/patogenicidade , Humanos , Intestinos/efeitos dos fármacos , Intestinos/microbiologia , Intestinos/fisiopatologia , Masculino , Metaplasia/tratamento farmacológico , Metaplasia/microbiologia , Metaplasia/fisiopatologia , Pessoa de Meia-Idade
9.
mBio ; 10(2)2019 03 19.
Artigo em Inglês | MEDLINE | ID: mdl-30890606

RESUMO

The gastric bacterium Helicobacter pylori causes a persistent infection that is directly responsible for gastric ulcers and gastric cancer in some patients and protective against allergic and other immunological disorders in others. The two outcomes of the Helicobacter-host interaction can be modeled in mice that are infected as immunocompetent adults and as neonates, respectively. Here, we have investigated the contribution of the Helicobacter immunomodulator VacA to H. pylori-specific local and systemic immune responses in both models. We found that neonatally infected mice are colonized at higher levels than mice infected as adults and fail to generate effector T-cell responses to the bacteria; rather, T-cell responses in neonatally infected mice are skewed toward Foxp3-positive (Foxp3+) regulatory T cells that are neuropilin negative and express RORγt. We found these peripherally induced regulatory T cells (pTregs) to be enriched, in a VacA-dependent manner, not only in the gastric mucosa but also in the lungs of infected mice. Pulmonary pTreg accumulation was observed in mice that have been infected neonatally with wild-type H. pylori but not in mice that have been infected as adults or mice infected with a VacA null mutant. Finally, we traced VacA to gastric lamina propria myeloid cells and show that it suppressed interleukin-23 (IL-23) expression by dendritic cells and induced IL-10 and TGF-ß expression in macrophages. Taken together, the results are consistent with the idea that H. pylori creates a tolerogenic environment through its immunomodulator VacA, which skews T-cell responses toward Tregs, favors H. pylori persistence, and affects immunity at distant sites.IMPORTANCE Helicobacter pylori has coexisted with humans for at least 60.000 years and has evolved persistence strategies that allow it to evade host immunity and colonize its host for life. The VacA protein is expressed by all H. pylori strains and is required for high-level persistent infection in experimental mouse models. Here, we show that VacA targets myeloid cells in the gastric mucosa to create a tolerogenic environment that facilitates regulatory T-cell differentiation, while suppressing effector T-cell priming and functionality. Tregs that are induced in the periphery during H. pylori infection can be found not only in the stomach but also in the lungs of infected mice, where they are likely to affect immune responses to allergens.


Assuntos
Proteínas de Bactérias/metabolismo , Diferenciação Celular , Mucosa Gástrica/patologia , Helicobacter pylori/imunologia , Membrana Mucosa/patologia , Células Mieloides/efeitos dos fármacos , Linfócitos T Reguladores/fisiologia , Animais , Células Dendríticas/imunologia , Modelos Animais de Doenças , Infecções por Helicobacter/patologia , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori/metabolismo , Evasão da Resposta Imune , Interleucina-10/metabolismo , Interleucina-23/metabolismo , Pulmão/patologia , Macrófagos/imunologia , Camundongos , Fator de Crescimento Transformador beta/metabolismo
10.
Hamostaseologie ; 39(3): 279-283, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30891714

RESUMO

There is an association between Helicobacter pylori infection and immune thrombocytopenia (ITP), and few studies have suggested that eradicative treatment of H. pylori infection may improve platelet counts in patients with ITP. Conventional treatments for ITP include immunosuppressive agents, and more recently thrombopoietic agents. However, based on clinical reports of association between H. pylori and ITP, several medical societies increasingly suggest detection and eradication of H. pylori as a treatment for ITP. In this article, we reappraise recent medical literature to determine the effectiveness of platelet response after treatment of H. pylori infection in patients with ITP. We searched two online databases (MEDLINE and Google Scholar) for full articles published between January 2008 and May 2018, and found a total of 11 studies that presented data and outcomes of treatment of H. pylori infection in ITP patients. All the studies administered triple therapy (amoxicillin 500 mg, clarithromycin 250 mg and a proton-pump inhibitor each given twice daily for either 7- or 14-day course) for eradication of H. pylori. Median overall platelet response ranged from 27 to 69.2% with a complete response rate ranging from 0 to 65.4% and a partial response rate ranging from 0 to 29.4%. Although there is variability in the effectiveness between different populations, it appears to be of benefit to ITP patients with concomitant H. pylori infection when treated with triple therapy. However, further studies to understand the pathogenesis of H. pylori-associated ITP is necessary for the development of new therapeutic approaches for ITP.


Assuntos
Plaquetas/efeitos dos fármacos , Infecções por Helicobacter/tratamento farmacológico , Púrpura Trombocitopênica Idiopática/tratamento farmacológico , Receptores de Trombopoetina/agonistas , Adulto , Amoxicilina/administração & dosagem , Amoxicilina/uso terapêutico , Antibacterianos/administração & dosagem , Antibacterianos/uso terapêutico , Plaquetas/imunologia , Claritromicina/administração & dosagem , Claritromicina/uso terapêutico , Quimioterapia Combinada , Feminino , Infecções por Helicobacter/complicações , Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori/efeitos dos fármacos , Helicobacter pylori/isolamento & purificação , Humanos , Imunossupressores/uso terapêutico , Masculino , Contagem de Plaquetas/tendências , Estudos Prospectivos , Inibidores da Bomba de Prótons/administração & dosagem , Inibidores da Bomba de Prótons/uso terapêutico , Púrpura Trombocitopênica Idiopática/complicações , Púrpura Trombocitopênica Idiopática/imunologia , Receptores de Trombopoetina/uso terapêutico , Estudos Retrospectivos , Resultado do Tratamento
11.
Minerva Gastroenterol Dietol ; 65(2): 116-129, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30759976

RESUMO

Helicobacter pylori (HP) is a gram-negative flagellated pathogen acid-resistant bacterium; it belongs to the order Campylobacterales that is wide spread all over the world, infecting more than 50% of the world population. HP infection is etiologically associated with non-atrophic and atrophic gastritis, peptic ulcer and with 3 to 6-fold increased relative risk for developing gastric adenocarcinoma and mucosa-associated lymphoid tissue (MA LT) lymphoma. For this reason HP is recognized by the World Health Organization as a Class I human carcinogen. In the last years a lot of studies clarified the role of this pathogen in nutrition and metabolism; particularly, it has been shown that it is able to induce malabsorption of several nutrients like iron, cobalamin, vitamin C and vitamin E, with strong consequences on nutritional status. Interesting, this bacterium is able to produce different biological effects on hormones like ghrelin and leptin controlling both appetite and growth, mostly depending on the time of acquisition of the infection and of its treatment. In this review, the authors focused their attention on nutritional effects of HP infection and particularly on the role that diet, food, plants and specific nutrients can play in its treatment, considering that HP eradication rates, with standard triple-therapy, have fallen to a low level in the last years.


Assuntos
Infecções por Helicobacter/fisiopatologia , Infecções por Helicobacter/terapia , Helicobacter pylori , Estado Nutricional , Infecções por Helicobacter/complicações , Humanos
12.
Crit Rev Microbiol ; 45(2): 239-251, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30776938

RESUMO

Epidemiological studies have shown that Helicobacter pylori (HP) infection is a risk factor for gastric cancer (GC). HP infection may induce the release of pro-inflammatory mediators, and abnormally increase the level of reactive oxygen species (ROS), nitric oxide (NO), and cytokines in mucosal epithelial cells of the stomach. However, the specific mechanism underlying the pathogenesis of HP-associated GC is still poorly understood. Recent studies have revealed that abnormal microRNA expression may affect the proliferation, differentiation, and apoptosis of mucosal epithelial cells of the stomach to further influence GC occurrence, development, and metastasis. Herein, we summarize the role of abnormal microRNAs in the regulation of HP-associated GC progression. Abnormal microRNA expression in HP-positive GC may be a biomarker for GC diagnosis, occurrence, and development as well as its targeted treatment and prognosis.


Assuntos
Infecções por Helicobacter/genética , Helicobacter pylori/fisiologia , MicroRNAs/genética , Neoplasias Gástricas/genética , Animais , Apoptose , Infecções por Helicobacter/metabolismo , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/fisiopatologia , Humanos , MicroRNAs/metabolismo , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/fisiopatologia
13.
Helicobacter ; 24(1): e12546, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30346636

RESUMO

BACKGROUND: Concomitant quadruple (CQT) or bismuth-containing quadruple therapy (BQT) is recommended as first-line treatment for Helicobacter pylori infection depending on antibiotic resistance. AIM: To compare the efficacy, safety, and compliance of CQT and BQT as first-line therapy for H. pylori eradication in real clinical practice in an area of high resistance to clarithromycin. METHODS: A prospective, open, comparative cross-sectional study including dyspeptic patients >18 years with H. pylori infection and with no previous eradication treatment was performed. CQT (omeprazole 20 mg + clarithromycin 500 mg + amoxicillin 1 g + metronidazole 500 mg, all given twice daily, for 14 days) or BQT (omeprazole 20 mg twice daily + 3 capsules of Pylera® 4 times a day, for 10 days) was prescribed at the discretion of the prescribing physician. Eradication was tested by 13 C-urea breath test. Efficacy was assessed by intention-to-treat (ITT) and per-protocol (PP) analyses. RESULTS: One hundred and four consecutive patients were included (64.4% female, age 52.9 years). Fifty patients received CQT and 54 BQT. Eradication rate was similar with both therapies at the PP (CQT 97.9%, 95% CI: 93.9-100 vs BQT 96.2%, 95% CI: 90.9-100, P = 0.605) and ITT analyses (CQT 98.0%, 95% CI: 94-100 vs BQT 94.4%, 95% CI: 88.1-100, P = 0.346). The rate of adverse events was also similar with CQT (56%) and BQT (46.3%). One patient in each group discontinued the treatment due to significant adverse events. CONCLUSION: The use of CQT and BQT as first-line treatment against H. pylori is similarly effective and safe strategy in an area of high clarithromycin resistance.


Assuntos
Antibacterianos/administração & dosagem , Bismuto/administração & dosagem , Farmacorresistência Bacteriana , Quimioterapia Combinada , Infecções por Helicobacter/tratamento farmacológico , Helicobacter pylori/efeitos dos fármacos , Claritromicina/farmacologia , Estudos Transversais , Esquema de Medicação , Quimioterapia Combinada/efeitos adversos , Feminino , Infecções por Helicobacter/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Resultado do Tratamento
14.
Int J Oncol ; 54(3): 916-928, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30569124

RESUMO

Evidence suggests that Helicobacter pylori (H. pylori) is not only the main cause of gastric cancer (GC), but is also closely associated with its metastasis. One of the major virulence factors in H. pylori is the cytotoxin­associated gene A (CagA). With the growing proportion of amoxicillin­resistant H. pylori strains, the present study aimed to explore the effects of CagA­ and penicillin­binding protein 1A (PBP1A) mutation­positive H. pylori (H. pyloriCagA+/P+) on GC cells, and its clinical significance. The clinical significance of H. pyloriCagA+/P+ infection was analyzed in patients with GC. In vitro, GC cells were infected with H. pyloriCagA+/P+ to investigate whether it was involved in the epithelial­mesenchymal transition (EMT) of SGC­7901 cells using immunofluorescence and western blot analysis. The results of clinical analysis demonstrated that, although CagA­negative H. pylori infection had no significant association with the characteristics of patients with GC, H. pyloriCagA+/P+ infection was significantly associated with various clinicopathological parameters, including invasion depth, lymphatic metastasis and distant metastasis. In vitro, the results indicated that H. pyloriCagA+/P+ promoted proliferation, invasion and EMT of SGC­7901 cells. MicroRNA (miR)­134 was downregulated in H. pyloriCagA+/P+ infected tissues compared with in those with H. pyloriCagA+/P­ infection. miR­134 overexpression significantly reversed H. pyloriCagA+/P+ infection­associated cell proliferation, invasion and EMT. Furthermore, the results revealed that Forkhead box protein M1 (FoxM1) was a direct target of miR­134, and FoxM1 knockdown impeded H. pyloriCagA+/P+­induced EMT. In conclusion, the present study demonstrated that miR­134 may suppress the proliferation, invasion and EMT of SGC­7901 cells by targeting FoxM1, and may serve a protective role in the process of H. pyloriCagA+/P+­induced GC. These findings may lead to an improved understanding of H. pyloriCagA+/P+­associated poor clinical characteristics in patients with GC.


Assuntos
Transição Epitelial-Mesenquimal , Infecções por Helicobacter/complicações , Helicobacter pylori/fisiologia , Interações Hospedeiro-Patógeno , MicroRNAs/genética , Proteínas de Ligação às Penicilinas/genética , Neoplasias Gástricas , Idoso , Antígenos de Bactérias/genética , Proteínas de Bactérias/genética , Linhagem Celular Tumoral , Proliferação de Células , Regulação para Baixo , Feminino , Proteína Forkhead Box M1/genética , Regulação Neoplásica da Expressão Gênica , Técnicas de Silenciamento de Genes , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori/genética , Humanos , Metástase Linfática , Masculino , MicroRNAs/metabolismo , Pessoa de Meia-Idade , Mutação , RNA Interferente Pequeno , Neoplasias Gástricas/etiologia , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/fisiopatologia
15.
Gastroenterol. latinoam ; 30(supl.1): S18-S25, 2019. ilus, tab, graf
Artigo em Espanhol | LILACS | ID: biblio-1116305

RESUMO

Helicobacter pylori (H. pylori) is a gram negative bacteria that survives in the gastric acid environment. The infection is acquired mainly during childhood. Fifty to 70% of adult population has the infection. However, in the last 10 year, a decrease in the prevalence of this infection has been observed in all age groups, in particular in pediatric population and elderly patients over 60 years old. The evolution of the infection depends on bacterial factors (virulence and toxins) and host immune response. People infected mainly develop gastrointestinal diseases such as gastritis, peptic ulcer and MALT lymphoma. H. pylori infection is the main risk factor of gastric cancer and for that reason, the eradication is recommended if H. pylori has been detected through invasive or non-invasive tests. Among children, eradication is not recommended unless there is a clinical manifestation that merits. H. pylori eradication is recommended in symptomatic adults and there is a controversy about massive eradication in asymptomatic population due to the risk of development of antibiotic resistance. Treatment is based on the use of proton pump inhibitors (PPI) associated to antibiotics, that should be chosen taking into account the increasing antibiotic resistance, and local availability. Clarithromycin (CLA) and levofloxacin resistance is increasingly high, and CLA-free quadruple therapy schemes are currently recommended for first-line therapy. H. pylori eradication must be confirmed with invasive or non-invasive tests. Second-line therapy based on antibiotics not previously used, PPI high doses and bismuth is recommended.


Helicobacter pylori (H. pylori) es una bacteria gramnegativa que sobrevive en el medio ácido gástrico. La infección se adquiere principalmente en la niñez. Un 50 a 70% de la población adulta es portadora, pero en los últimos 10 años, se ha observado una disminución en la prevalencia de infección en todos los grupos etarios, en particular en población pediátrica y mayores de 60 años. La evolución de la infección depende de factores propios de la bacteria (virulencia, toxinas) y de la respuesta inmune del huésped. Los individuos infectados desarrollan principalmente patologías gastrointestinales como gastritis, úlcera péptica y linfoma MALT. La infección por H. pylori es el principal factor de riesgo del cáncer gástrico por lo que se recomienda su erradicación en caso de haberse detectado mediante test invasivo o no invasivo. En niños, no es recomendable la erradicación a menos que exista una manifestación clínica que lo amerite. Se recomienda su erradicación en adultos sintomáticos y existe controversia respecto a la erradicación masiva en población asintomática debido al riesgo de desarrollar resistencia antibiótica. El tratamiento se basa en el uso de inhibidores de la bomba de protones asociado a antibióticos, los cuales deben ser escogidos teniendo en cuenta la tasa de resistencia antimicrobiana y disponibilidad local. La resistencia a claritromicina (CLA) y levofloxacino es creciente, por lo que se recomienda el uso de esquemas de cuadriterapia libre de CLA en esquemas de primera línea. Se recomienda confirmar su erradicación con test no invasivos y retratar con esquema de segunda línea con antibióticos no utilizados previamente, asociado a dosis altas de inhibidores de bomba de protones y sales de bismuto.


Assuntos
Humanos , Criança , Adulto , Infecções por Helicobacter/tratamento farmacológico , Indução de Remissão , Helicobacter pylori/efeitos dos fármacos , Helicobacter pylori/patogenicidade , Infecções por Helicobacter/diagnóstico , Infecções por Helicobacter/fisiopatologia , Fatores Etários , Claritromicina/uso terapêutico , Farmacorresistência Bacteriana/efeitos dos fármacos , Quimioterapia Combinada , Inibidores da Bomba de Prótons/uso terapêutico , Levofloxacino/uso terapêutico
16.
Acta Clin Croat ; 58(4): 576-582, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32595240

RESUMO

Helicobacter pylori (H. pylori) is a common problem and a significant cause of chronic gastric inflammation. H. pylori, ongoing gastric inflammation and its severity are the most critical component of precursors of gastric cancer. Hypothetically, every chronic tissue injury activates platelets, and the mean platelet volume (MPV) reflects this action well. The potential relationship between H. pylori and platelet count has been shown before. However, there are few and conflicting papers about the relationship between MPV and H. pylori related chronic gastric inflammation and its severity. The study aimed to assess any potential relationship between MPV and presence of H. pylori, as well as the severity of chronic gastric inflammation. A total of 6890 endoscopic reports were initially evaluated, and a total of 218 dyspeptic patients having undergone upper endoscopy were included. Of these, 118 (54.2%) were H. pylori positive and 100 (45.8%) were H. pylori negative. At least four gastric biopsies were obtained and evaluated according to Sydney classification. Age, gender, hemoglobin, mean corpuscular volume, ferritin, serum iron and C-reactive protein, as well as endoscopic findings were also recorded. A p<0.05 was accepted as significant. The MPV and platelet count did not differ between H. pylori positive and H. pylori negative groups of patients (p>0.05). There were no differences and correlation between MPV and gastric inflammation severity according to Sydney classification (p>0.05). When stratifying MPV as <9.15 fL and >9.15 fL, there was no difference between H. pylori positive and H. pylori negative groups either (p>0.05). In this study, we found no relationship between MPV and presence of H. pylori or severity of gastric inflammation. Although there are still conflicting publications on this issue, in our opinion and according to the results of this study, MPV is not a suitable marker for evaluation of gastric inflammation severity, being H. pylori either positive or negative.


Assuntos
Biomarcadores/sangue , Plaquetas/patologia , Gastrite/sangue , Gastrite/fisiopatologia , Infecções por Helicobacter/sangue , Infecções por Helicobacter/fisiopatologia , Volume Plaquetário Médio , Adulto , Idoso , Idoso de 80 Anos ou mais , Biópsia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade
17.
Acta Biomed ; 89(9-S): 81-86, 2018 12 17.
Artigo em Inglês | MEDLINE | ID: mdl-30561399

RESUMO

BACKGROUND: Inflammatory bowel diseases (IBD), are chronic, relapsing-remitting diseases of the gastrointestinal tract, including Crohn's disease (CD), Ulcerative colitis (UC) and Unclassified IBD (IBDU). Their pathogenesis involves genes and environment as cofactors in inducing autoimmunity; particularly the interactions between enteric pathogens and immunity is being studied. Helicobacter pylori (HP) is common pathogen causing gastric inflammation. Studies found an inverse prevalence association between HP and IBD, suggesting a potential protecting role of HP from IBD. METHODS: A literature search of the PubMed database was performed using the key words ''helicobacter pylori'', ''inflammatory bowel disease'', ''crohn disease'', "ulcerative colitis". Embase, Medline (OvidSP), Web of Science, Scopus, PubMed publisher, Cochrane and Google Scholar were also searched. Prevalence rate-ratios among HP in IBD patients, HP in CD patients, HP in UC patients, HP in IBDU patients were extracted, each group was compared with controls, to verify the inverse association between HP and IBD prevalence. RESULTS: In all groups the dispersion of data suggested an inverse association between IBD group and controls, even when the comparison was carried out separately between each group of newly diagnosed patients and controls, to rule out the possible bias of ongoing pharmacologic therapy. CONCLUSIONS: The results of this review show a striking inverse association between HP infection and the prevalence of IBD, independently from the type of IBD considered across distinct geographic regions. Anyway, data should be interpreted cautiously, as wider, prospective and more homogeneous research on this topic are awaited, which could open new scenarios about environmental etiology of IBD.


Assuntos
Gastrite/epidemiologia , Infecções por Helicobacter/epidemiologia , Helicobacter pylori , Doenças Inflamatórias Intestinais/epidemiologia , Comorbidade , Disbiose/complicações , Gastrite/imunologia , Gastrite/microbiologia , Gastrite/fisiopatologia , Saúde Global , Infecções por Helicobacter/imunologia , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori/imunologia , Helicobacter pylori/fisiologia , Humanos , Prevalência
18.
J Biomed Sci ; 25(1): 68, 2018 Sep 11.
Artigo em Inglês | MEDLINE | ID: mdl-30205817

RESUMO

Although most H. pylori infectors are asymptomatic, some may develop serious disease, such as gastric adenocarcinoma, gastric high-grade B cell lymphoma and peptic ulcer disease. Epidemiological and basic studies have provided evidence that infection with H. pylori carrying specific virulence factors can lead to more severe outcome. The virulence factors that are associated with gastric adenocarcinoma development include the presence, expression intensity and types of cytotoxin-associated gene A (CagA, especially EPIYA-D type and multiple copies of EPIYA-C) and type IV secretion system (CagL polymorphism) responsible for its translocation into the host cells, the genotypes of vacuolating cytotoxin A (vacA, s1/i1/m1 type), and expression intensity of blood group antigen binding adhesin (BabA, low-producer or chimeric with BabB). The presence of CagA is also related to gastric high-grade B cell lymphoma occurrence. Peptic ulcer disease is closely associated with cagA-genopositive, vacA s1/m1 genotype, babA2-genopositive (encodes BabA protein), presence of duodenal ulcer promoting gene cluster (dupA cluster) and induced by contact with epithelium gene A1 (iceA1), and expression status of outer inflammatory protein (OipA). The prevalence of these virulence factors is diverse among H. pylori isolated from different geographic areas and ethnic groups, which may explain the differences in disease incidences. For example, in East Asia where gastric cancer incidence is highest worldwide, almost all H. pylori isolates were cagA genopositive, vacA s1/i1/m1 and BabA-expressing. Therefore, selection of appropriate virulence markers and testing methods are important when using them to determine risk of diseases. This review summarizes the evidences of H. pylori virulence factors in relation with gastroduodenal diseases and discusses the geographic differences and appropriate methods of analyzing these virulence markers.


Assuntos
Gastroenteropatias/fisiopatologia , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori/fisiologia , Fatores de Virulência/fisiologia , Gastroenteropatias/microbiologia , Infecções por Helicobacter/microbiologia
20.
Sci Rep ; 8(1): 14180, 2018 09 21.
Artigo em Inglês | MEDLINE | ID: mdl-30242291

RESUMO

The aim is to determine whether there is an independent association between Hp infection and carotid intima-media thickness (CIMT) in a cross-section observational study. Among of 14588 routine health check-up participants, 13770 subjects underwent the 13C-urea breath test (13C-UBT) and ultrasound measurement of CIMT. Traditional atherosclerotic risk factors were also recorded. The ratio of increased CIMT in Hp positive group (28.6%) was not significant difference compared with Hp negative group (29.7%) (p = 0.164). The HP infection rates was no significant difference between increased CIMT (38.4%) and non- increased CIMT (39.7%) patients. However, all the traditional atherosclerotic risk factors including age, gender, BMI, waistline, total cholesterol, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, high density lipoprotein cholesterol, triglycerides, free fatty acid, homocysteine, systolic and diastolic blood pressure, fasting plasma glucose and C reactive protein were different between increased CIMT and non- increased CIMT participants. The odds of Hp infection for CIMT risk (OR 0.948; 95% CI 0.879-1.022; P = 0.164) was not higher in binary logistic regression analysis even after adjustment for traditional risk factors (OR 1.118; 95% CI 0.958-1.306; P = 0.157). Our study found no evidence of association between CIMT and HP infection.


Assuntos
Doenças das Artérias Carótidas/etiologia , Doenças das Artérias Carótidas/fisiopatologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/fisiopatologia , Aterosclerose/sangue , Aterosclerose/etiologia , Aterosclerose/metabolismo , Aterosclerose/fisiopatologia , Proteína C-Reativa/metabolismo , Doenças das Artérias Carótidas/sangue , Doenças das Artérias Carótidas/metabolismo , Espessura Intima-Media Carotídea , HDL-Colesterol/sangue , LDL-Colesterol/sangue , VLDL-Colesterol/sangue , Estudos Transversais , Feminino , Infecções por Helicobacter/sangue , Infecções por Helicobacter/metabolismo , Helicobacter pylori/patogenicidade , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Triglicerídeos/sangue
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