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1.
BMJ Case Rep ; 14(7)2021 Jul 09.
Artigo em Inglês | MEDLINE | ID: mdl-34244191

RESUMO

Helicobacter pylori infection could cause chronic inflammation in the stomach and induce peptic ulcer disease or even malignant tumour. The initial infection of the organism happens in childhood but most of cases are latent. We had a case of 10-year-old girl who presented with acute epigastric pain and significant thickening of the stomach wall on CT. The finding seemed atypical for acute gastritis so oesophagogastroduodenoscopy and serology examination were added and the primary infection of H. pylori was confirmed with the exclusion of other possible diagnoses like eosinophilic gastritis and IgA vasculitis. Acute gastritis is one of the most common sickness in children, however, it would be worthwhile considering further investigation including H. pylori infection in a case of atypical presentation to prevent negative consequences derived from chronic H. pylori infection.


Assuntos
Gastrite , Infecções por Helicobacter , Helicobacter pylori , Úlcera Péptica , Criança , Feminino , Gastrite/diagnóstico , Infecções por Helicobacter/complicações , Infecções por Helicobacter/diagnóstico , Humanos
2.
Int J Mol Sci ; 22(13)2021 Jun 29.
Artigo em Inglês | MEDLINE | ID: mdl-34209478

RESUMO

The antral hormone gastrin potently regulates gastric acid secretion and fundic mucosal growth. Consequently, appropriate gastrin secretion and plasma concentrations are important for the early phases of digestion. This review describes as the first premise the normal biogenesis of gastrin in the antral mucosa, but also mentions the extraantral expression. Subsequently, the molecular nature and concentration levels of gastrin in serum or plasma are overviewed. Third, assays for accurate measurements of plasma or serum concentrations are commented. Finally, the problem of moderate hypergastrinemia due to Helicobacter pylori infections and/or treatment with proton-pump inhibitors (PPI) is discussed. The review concludes that accurate measurement of the true concentrations of bioactive gastrins in plasma is important. Moreover, it suggests that moderate hypergastrinemias are also essential health issues that require serious attention.


Assuntos
Suscetibilidade a Doenças/sangue , Suscetibilidade a Doenças/etiologia , Gastrinas/metabolismo , Animais , Biomarcadores , Mucosa Gástrica/metabolismo , Mucosa Gástrica/patologia , Células Secretoras de Gastrina/metabolismo , Gastrinas/sangue , Gastrinas/química , Gastrinas/genética , Regulação da Expressão Gênica , Infecções por Helicobacter/complicações , Infecções por Helicobacter/microbiologia , Helicobacter pylori/fisiologia , Humanos , Técnicas de Diagnóstico Molecular , Especificidade de Órgãos/genética , Inibidores da Bomba de Prótons/efeitos adversos , Inibidores da Bomba de Prótons/uso terapêutico , Kit de Reagentes para Diagnóstico
3.
Medicine (Baltimore) ; 100(27): e26418, 2021 Jul 09.
Artigo em Inglês | MEDLINE | ID: mdl-34232174

RESUMO

BACKGROUND: Previous studies have demonstrated that Helicobacter pylori is a critical factor in the development of gastrointestinal diseases. However, only limited studies have reported results on the relationship between H pylori infection and patients with type 2 diabetes mellitus (T2DM). Moreover, the conclusions from these past studies are variable. Because there are contradictory results on this issue, the present study aims to examine the clinical therapeutic impacts of H pylori eradication to treat patients experiencing T2DM. METHODS: The present protocol is drafted according to the provisions of the Preferred Reporting Items for Systematic Review and Meta-analyses Protocols guidelines. PubMed, Cochrane Central Register of Controlled Trials databases, EMBASE, Web of Science, China National Knowledge Infrastructure, and Chinese BioMedical Literature Database will be searched up to May 2021 to obtain randomized controlled trials evaluating the clinical therapeutic effects of H pylori eradication to treat patients experiencing T2DM. We will use 2 investigators independently to carry out study selection, data extraction, and employ the Cochrane Collaboration criteria to evaluate their risks of bias. Furthermore, we will apply Stata 16.0 software to perform data analysis. RESULTS: We intend to evaluate the clinical therapeutic impacts of H pylori eradication to treat patients suffering from T2DM. CONCLUSIONS: Our findings may support existing evidence on the clinical therapeutic impacts of H pylori eradication to treat patients with T2DM. ETHICS AND DISSEMINATION: Since all data will be extracted from the published literature, the study does not require an ethical approval. OSF REGISTRATION NUMBER: May 31, 2021.osf.io/qtexu. (https://osf.io/qtexu/).


Assuntos
Diabetes Mellitus Tipo 2/tratamento farmacológico , Medicamentos de Ervas Chinesas/uso terapêutico , Infecções por Helicobacter/tratamento farmacológico , Helicobacter pylori/isolamento & purificação , Diabetes Mellitus Tipo 2/complicações , Infecções por Helicobacter/complicações , Humanos
4.
Medicine (Baltimore) ; 100(26): e26336, 2021 Jul 02.
Artigo em Inglês | MEDLINE | ID: mdl-34190151

RESUMO

ABSTRACT: We aimed to determine the clinical characteristics and prognosis factors of young patients with gastric cancer (GC).A total of 101 young patients with GC referred to Zhengzhou University People's Hospital, Henan province, China between January 1st, 2003 and June 1st, 2015 were retrospectively reviewed. The medical records included ages, genders, marital status, family history of tumors, comorbidity, Helicobacter pylori (H.pylori) infection, fibrinogen, prealbumin, alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), tumor location, tumor size, TNM stage, differentiation of the tumor, WHO type, treatment method and prognostic factors effect were further assessed.The mean age of GC patients in our group was 26.0 years. The incidence was slightly higher in females (female: male = 1.1:1). Some patients had the family history of tumor and H.pylori infection (2.0%, 6.9%). The tumor sizes were mainly under 5 cm (52.4%) and the most locations were in the antrum (43.5%) and body (42.5%). A large number of patients were diagnosed as adenocarcinomas (66.3%) and the main histological of GC was poor differentiated (72.3%). Moreover, a high proportion of patients were diagnosed at the stages III-IV (61.4%), and most patients received surgery combined chemotherapy (63.4%), however, the survival outcome was poor. In univariate Cox analysis, tumor sizes, TNM stage were significantly associated with overall survival (OS) and the multivariate Cox analysis demonstrated that TNM stage was significantly associated with OS.GC in young patients has its unique biological and clinical features. A large majority of young patients were diagnosed at their advanced stages with poor prognostic. TNM stage was an independent prognostic factor for young patients with GC, early GC screening in young people should be actively promoted.


Assuntos
Neoplasias Gástricas/patologia , Adenocarcinoma/complicações , Adenocarcinoma/mortalidade , Adenocarcinoma/patologia , Adolescente , Adulto , Idade de Início , Biomarcadores Tumorais/sangue , Carcinoma de Células em Anel de Sinete/complicações , Carcinoma de Células em Anel de Sinete/mortalidade , Carcinoma de Células em Anel de Sinete/patologia , China/epidemiologia , Feminino , Predisposição Genética para Doença , Infecções por Helicobacter/complicações , Humanos , Masculino , Gradação de Tumores , Metástase Neoplásica , Estadiamento de Neoplasias , Prognóstico , Modelos de Riscos Proporcionais , Estudos Retrospectivos , Neoplasias Gástricas/complicações , Neoplasias Gástricas/mortalidade , Carga Tumoral , Adulto Jovem
5.
Pol J Pathol ; 72(1): 87-88, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34060292

RESUMO

We read with great interest the review article "Lymphocytic gastritis" by Puderecki et al., which was recently published in your journal [1]. The article describes the features of lymphocytic gastritis (LG), a rare form of gastritis with unclear pathogenesis. The diagnosis of LG is based on histology which reveals intraepithelial lymphocytosis (> 25 intraepithelial lymphocytes per 100 gastric surface and foveolar epithelial cells). The endoscopic appearance of LG can vary from normal mucosa to aphthous erosions, nodularity, local spots, polyps, and ulcers. The most common locations of the lesions are the body and the antrum. With regard to etiology, Celiac disease (CD) is the main reported cause of LG, followed by Helicobacter pylori infection. After a careful review of the argument, Puderecki et al. conclude that there is no one exact cause of LG, and rather than being a separate disease, LG is more likely a sign of the disease with which it is associated [1]. We wrote to remark on the strong connection between LG and CD. Such a connection may allow some etiopathogenetic and clinical speculations.


Assuntos
Doença Celíaca , Gastrite , Infecções por Helicobacter , Helicobacter pylori , Mucosa Gástrica , Infecções por Helicobacter/complicações , Humanos
6.
Clin J Gastroenterol ; 14(4): 947-954, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34018155

RESUMO

BACKGROUND: Mucosal atrophy and enlarged folds of stomach by double-contrast upper gastrointestinal barium X-ray radiography (UGI-XR) are two major features of Helicobacter pylori-induced chronic gastritis. These were previously shown to be risk indicators of gastric cancer, but their predictability for clinicopathological characters of developed gastric cancer is unelucidated. In addition, evidence for decreasing the mortality of gastric cancer by appropriate follow-up of UGI screening is needed. METHODS: The 5134 generally healthy UGI-XR examinees, who underwent follow-up UGI-XR or upper gastrointestinal endoscopy (UGI-ES) more than once, were prospectively observed for 10 years. RESULTS: At the beginning of follow-up, 1515 (29.5%) had mucosal atrophy and 990 (19.5%) had enlarged folds. For the serum anti-H. pylori IgG, 1301 (25.3%) were positive, 177 (3.4%) were possibly positive, and 3656 (71.2%) were negative. During the 10-year observation period, gastric cancer developed in 15 subjects, among which 13 had mucosal atrophy and 10 had enlarged folds. These two features were expectedly useful indicators for gastric cancer incidence, but they showed no significant association with tumor stage or histological type of developed cancer. Only one of the 5134 subjects died of gastric cancer during 10 years, which was significantly lower than the predicted number of gastric cancer death (6.78 for 10 years) according to the mortality rate in Japan. CONCLUSIONS: Neither mucosal atrophy nor enlarged folds of stomach showed a significant association with clinicopathological features of developed gastric tumors. Appropriate follow-up of cancer screening by UGI-XR or UGI-ES can reduce the risk of gastric cancer-related death.


Assuntos
Infecções por Helicobacter , Helicobacter pylori , Neoplasias Gástricas , Atrofia/patologia , Bário , Mucosa Gástrica/diagnóstico por imagem , Mucosa Gástrica/patologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/diagnóstico por imagem , Humanos , Japão , Prognóstico , Radiografia , Neoplasias Gástricas/diagnóstico por imagem , Neoplasias Gástricas/patologia , Raios X
7.
Medicine (Baltimore) ; 100(21): e26091, 2021 May 28.
Artigo em Inglês | MEDLINE | ID: mdl-34032746

RESUMO

INTRODUCTION: This work reports a patient with recurrent renal calculi subjected to three surgeries in half a year to be in the same position, and the high-throughput sequencing data showed different species in the renal pus and urine samples, which suggested that partial renal infection or stone formation can be judged by the bacteria in urine. PATIENT CONCERNS: The female patient aged 43 years was referred to the authors' department on April 13, 2020, due to left waist pain and fever for 3 days. DIAGNOSIS: Kidney stones and hydronephrosis were determined by a urinary system computed tomography scan. INTERVENTIONS: On April 20, 2020 and June 15, 2020, the patient was successfully treated with left percutaneous nephrolithotomy twice under general anesthesia. An investigation on the health and eating habits of the patient within 6 months was completed at the last admission. The components of the second renal calculus sample were analyzed with an infrared spectrum analyzer. The third renal stone (renal pus, triplicates) was subjected to microbial metagenome sequencing, and urine samples before and after surgery were subjected to 16S RNA sequencing by SEQHEALTH (Wuhan, China). OUTCOMES: After percutaneous nephrolithotomy, the left kidney stones were basically cleared, stone analysis revealed that the main components were calcium oxalate monohydrate, silica, and a small amount of calcium oxalate dehydrate. Although the urine samples exhibited differences, the renal pus and urine sample shared a single species. CONCLUSION: It is not clear that the prospects of partial renal infection or stone formation can be judged by the bacteria in urine.


Assuntos
Infecções por Helicobacter/diagnóstico , Hidronefrose/diagnóstico , Cálculos Renais/diagnóstico , Nefrolitotomia Percutânea/efeitos adversos , Infecções Urinárias/diagnóstico , Adulto , DNA Bacteriano/isolamento & purificação , Feminino , Infecções por Helicobacter/complicações , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/cirurgia , Helicobacter pylori , Humanos , Hidronefrose/microbiologia , Hidronefrose/cirurgia , Cálculos Renais/microbiologia , Cálculos Renais/cirurgia , Metagenoma/genética , RNA Ribossômico 16S/genética , Recidiva , Reoperação , Infecções Urinárias/complicações , Infecções Urinárias/microbiologia , Infecções Urinárias/cirurgia
8.
J Med Case Rep ; 15(1): 308, 2021 May 30.
Artigo em Inglês | MEDLINE | ID: mdl-34051825

RESUMO

BACKGROUND: Membranous nephropathy (MN) is the leading cause of nephrotic syndrome in adults worldwide. A growing body of evidence indicates a pathogenic and autoimmune correlation between Helicobacter pylori infection, MN, and autoimmune liver disease. CASE PRESENTATION: A 47-year-old African American woman presented to our institution with epigastric pain and vomiting. In-patient hospital workup included a thorough abdominal evaluation including esophagogastroduodenoscopy and liver biopsy, which revealed active H. pylori infection and autoimmune hepatitis. The patient was incidentally also found to have nephrotic-range proteinuria. Renal workup including kidney biopsy established the diagnosis of MN. Proteinuria improved after initiation of triple therapy for H. pylori infection. CONCLUSION: This case adds to the growing evidence of a correlation between H. pylori infection, MN, and autoimmune liver disease. This report demonstrates a unique case of a patient with MN, autoimmune hepatitis (AIH)/primary biliary cholangitis (PBC), and HP who underwent triple-eradication antibiotic treatment that resulted in an ultimate resolution of all these conditions.


Assuntos
Glomerulonefrite Membranosa , Infecções por Helicobacter , Helicobacter pylori , Hepatite Autoimune , Adulto , Feminino , Glomerulonefrite Membranosa/complicações , Glomerulonefrite Membranosa/diagnóstico , Glomerulonefrite Membranosa/tratamento farmacológico , Infecções por Helicobacter/complicações , Infecções por Helicobacter/diagnóstico , Infecções por Helicobacter/tratamento farmacológico , Hepatite Autoimune/complicações , Hepatite Autoimune/diagnóstico , Hepatite Autoimune/tratamento farmacológico , Humanos , Rim , Pessoa de Meia-Idade
9.
Artigo em Inglês | MEDLINE | ID: mdl-33975683

RESUMO

Gastric carcinogenesis can be described as a consequence of multilevel molecular alterations that is triggered by a cascade of events. Historically, diet and environmental factors have been identified to substantially contribute to carcinogenesis before the discovery of Helicobacter pylori (H. pylori). But H. pylori infection has revolutionized the understanding of gastric carcinogenesis. Although the model of H. pylori-driven carcinogenesis remains valid, there is a continuous effort to precisely delineate the molecular pathways involved and to understand the interplay with additional risk factors including recent relevant knowledge on the stomach microbiota. In this review, we provide an updated view on the models of gastric carcinogenesis. This includes historically appreciated H. pylori-induced models and expands these taking recent molecular data into consideration. Based on the data provided, we conclude that indeed H. pylori-carcinogenesis remains one of the best-established models at least for a subset of gastric cancers. Implementation of the recently identified molecular subtypes in novel genetic animal models is required to expand our knowledge on H. pylori-independent carcinogenesis.


Assuntos
Infecções por Helicobacter/complicações , Helicobacter pylori/patogenicidade , Neoplasias Gástricas/virologia , Animais , Humanos , Camundongos , Modelos Moleculares
10.
Artigo em Inglês | MEDLINE | ID: mdl-33975687

RESUMO

Gastric cancer remains a major challenge to public health on a global scale, causing the loss of 19 million disability-adjusted life years worldwide in 2017. The future burden will increase due to population growth and ageing. Considering its absolute burden and persisting disparities, in addition to the substantial prevalence of Helicobacter pylori infection worldwide that is treatable, gastric cancer is a logical target for urgent global action for prevention. In this review, we discuss recent progress in gastric cancer prevention and propose a concerted international effort to implement population-based H. pylori treatment programmes, as the best evidence-based strategy that is currently available for gastric cancer prevention, in the context of demonstration projects in selected populations, to be later scaled up. It is time for urgent action to reduce the important loss of life and productivity caused by this preventable malignancy.


Assuntos
Infecções por Helicobacter/complicações , Neoplasias Gástricas/prevenção & controle , Humanos , Neoplasias Gástricas/epidemiologia
11.
Medicine (Baltimore) ; 100(20): e26045, 2021 May 21.
Artigo em Inglês | MEDLINE | ID: mdl-34011117

RESUMO

OBJECTIVE: The effect of Helicobacter pylori (H pylori) eradication therapy in functional dyspepsia (FD) patients was inconsistent in previously published randomized controlled trials. Therefore, we performed a comprehensive protocol for systematic review and meta-analysis in order to assess whether H pylori eradication therapy benefits patients with FD. METHODS: In this systematic review and meta-analysis, we will search Web of Science, Embase, PubMed, Wanfang Data, Medline, Science Direct, Cochrane Library through April, 2021. The protocol was written following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols. Data extraction was performed independently and only randomized clinical trials were included in this study. The risk of bias assessment was performed using the tool recommended in the Cochrane Handbook for Systematic Reviews of Interventions. All calculations were carried out with Stata 11.0 (The Cochrane Collaboration, Oxford, United Kingdom). RESULTS: We hypothesized that H pylori eradication therapy compared to no eradication therapy has a statistically significant benefit for symptom relief and can also reduce the development of peptic ulcer disease. CONCLUSION: This study expects to provide credible and scientific evidence for the efficacy of H pylori eradication therapy for patients with FD. OSF REGISTRATION NUMBER: 10.17605/OSF.IO/4EHRB.


Assuntos
Dispepsia/prevenção & controle , Infecções por Helicobacter/tratamento farmacológico , Helicobacter pylori , Dispepsia/microbiologia , Infecções por Helicobacter/complicações , Humanos
12.
Jpn J Clin Oncol ; 51(7): 1158-1170, 2021 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-33893508

RESUMO

BACKGROUND: In Japan, there are ongoing efforts to shift the gastric cancer prevention and control policy priorities from barium-based screening to Helicobacter pylori (H. pylori)-oriented primary prevention. A comprehensive summary of the evidence regarding the effects of H. pylori eradication on the risk of gastric cancer could inform policy decisions. METHODS: We conducted a systematic review and meta-analysis of published studies evaluating the effectiveness of H. pylori eradication for the prevention of gastric cancer in otherwise healthy individuals (primary prevention) and early gastric cancer patients (tertiary prevention). RESULTS: In total, 19 studies were included. Three moderate-quality observational cohort studies showed that H. pylori eradication may be associated with a decreased risk of gastric cancer in healthy asymptomatic Japanese people. There is moderate certainty regarding the effectiveness of H. pylori eradication in patients with gastrointestinal diseases, such as peptic ulcers. A meta-analysis of 10 observational studies with otherwise healthy individuals (mainly peptic ulcer patients) yielded an overall odds ratio of 0.34 (95% CI: 0.25-0.46). Regarding tertiary prevention, the overall odds ratio for developing metachronous gastric cancer was 0.42 (95% CI: 0.35-0.51) in the eradication group in a meta-analysis of nine studies involving early gastric cancer patients who underwent endoscopic resection. CONCLUSION: H. pylori eradication is effective in preventing gastric cancer in the Japanese population, regardless of symptoms. Well-designed, large cohort studies are warranted to determine the long-term efficacy and safety of H. pylori eradication in the context of reducing the gastric cancer burden through population-based screening and treatment.


Assuntos
Infecções por Helicobacter/epidemiologia , Helicobacter pylori , Neoplasias Gástricas/epidemiologia , Infecções por Helicobacter/complicações , Humanos , Incidência , Japão/epidemiologia , Razão de Chances , Neoplasias Gástricas/etiologia , Neoplasias Gástricas/prevenção & controle
13.
Int J Mol Sci ; 22(7)2021 Mar 26.
Artigo em Inglês | MEDLINE | ID: mdl-33810350

RESUMO

Gastric cancer's bad incidence, prognosis, cellular and molecular heterogeneity amongst others make this disease a major health issue worldwide. Understanding this affliction is a priority for proper patients' management and for the development of efficient therapeutical strategies. This review gives an overview of major scientific advances, made during the past 5-years, to improve the comprehension of gastric adenocarcinoma. A focus was made on the different actors of gastric carcinogenesis, including, Helicobacter pylori cancer stem cells, tumour microenvironment and microbiota. New and recent potential biomarkers were assessed as well as emerging therapeutical strategies involving cancer stem cells targeting as well as immunotherapy. Finally, recent experimental models to study this highly complex disease were discussed, highlighting the importance of gastric cancer understanding in the hard-fought struggle against cancer relapse, metastasis and bad prognosis.


Assuntos
Adenocarcinoma/metabolismo , Carcinogênese , Neoplasias Gástricas/metabolismo , Animais , Biomarcadores/metabolismo , Biomarcadores Tumorais , Linhagem Celular Tumoral , Infecções por Helicobacter/complicações , Helicobacter pylori , Humanos , Imunoterapia , Biópsia Líquida , Camundongos , Metástase Neoplásica , Recidiva Local de Neoplasia/patologia , Células-Tronco Neoplásicas/citologia , Prognóstico , Recidiva , Fatores de Risco , Neoplasias Gástricas/microbiologia , Microambiente Tumoral
14.
Cell Mol Life Sci ; 78(10): 4765-4783, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33825941

RESUMO

Infection with H. pylori induces a strong host cellular response represented by induction of a set of molecular signaling pathways, expression of proinflammatory cytokines and changes in proliferation. Chronic infection and inflammation accompanied by secretory dysfunction can result in the development of gastric metaplasia and gastric cancer. Currently, it has been determined that the regulation of many cellular processes involves ubiquitinylation of molecular effectors. The binding of ubiquitin allows the substrate to undergo a change in function, to interact within multimolecular signaling complexes and/or to be degraded. Dysregulation of the ubiquitinylation machinery contributes to several pathologies, including cancer. It is not understood in detail how H. pylori impacts the ubiquitinylation of host substrate proteins. The aim of this review is to summarize the existing literature in this field, with an emphasis on the role of E3 ubiquitin ligases in host cell homeodynamics, gastric pathophysiology and gastric cancer.


Assuntos
Infecções por Helicobacter/metabolismo , Helicobacter pylori/patogenicidade , Neoplasias Gástricas/metabolismo , Ubiquitina/metabolismo , Animais , Mucosa Gástrica/metabolismo , Mucosa Gástrica/microbiologia , Infecções por Helicobacter/complicações , Humanos , Transdução de Sinais/fisiologia , Neoplasias Gástricas/etiologia , Neoplasias Gástricas/microbiologia , Ubiquitina-Proteína Ligases/metabolismo
15.
Toxins (Basel) ; 13(5)2021 04 28.
Artigo em Inglês | MEDLINE | ID: mdl-33924897

RESUMO

Although millions of people have been infected by Helicobacter pylori (H. pylori), only a small proportion of infected individuals will develop adverse outcomes, ranging from chronic gastritis to gastric cancer. Advanced development of the disease has been well-linked with chronic inflammation, which is significantly impacted by the adaptive and humoral immunity response. From the perspective of cellular immunity, this review aims to clarify the intricate axis between IL-17, IL-21, and IL-23 in H. pylori-related diseases and the pathogenesis of inflammatory gastrointestinal diseases. CD4+ helper T (Th)-17 cells, with the hallmark pleiotropic cytokine IL-17, can affect antimicrobial activity and the pathogenic immune response in the gut environment. These circumstances cannot be separated, as the existence of affiliated cytokines, including IL-21 and IL-23, help maintain Th17 and accommodate humoral immune cells. Comprehensive understanding of the dynamic interaction between molecular host responses in H. pylori-related diseases and the inflammation process may facilitate further development of immune-based therapy.


Assuntos
Gastrite/etiologia , Infecções por Helicobacter/patologia , Helicobacter pylori , Interleucina-17/metabolismo , Interleucina-23/metabolismo , Interleucinas/metabolismo , Gastrite/metabolismo , Gastrite/microbiologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/metabolismo , Humanos
16.
Toxins (Basel) ; 13(3)2021 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-33804551

RESUMO

The tumor necrosis factor-α (TNF-α)-inducing protein (tipα) gene family, comprising Helicobacter pylori membrane protein 1 (hp-mp1) and tipα, has been identified as a tumor promoter, contributing to H. pylori carcinogenicity. Tipα is a unique H. pylori protein with no similarity to other pathogenicity factors, CagA, VacA, and urease. American H. pylori strains cause human gastric cancer, whereas African strains cause gastritis. The presence of Tipα in American and Euro-Asian strains suggests its involvement in human gastric cancer development. Tipα secreted from H. pylori stimulates gastric cancer development by inducing TNF-α, an endogenous tumor promoter, through its interaction with nucleolin, a Tipα receptor. This review covers the following topics: tumor-promoting activity of the Tipα family members HP-MP1 and Tipα, the mechanism underlying this activity of Tipα via binding to the cell-surface receptor, nucleolin, the crystal structure of rdel-Tipα and N-terminal truncated rTipα, inhibition of Tipα-associated gastric carcinogenesis by tumor suppressor B-cell translocation gene 2 (BTG2/TIS21), and new strategies to prevent and treat gastric cancer. Thus, Tipα contributes to the carcinogenicity of H. pylori by a mechanism that differs from those of CagA and VacA.


Assuntos
Antígenos de Bactérias/metabolismo , Proteínas da Membrana Bacteriana Externa/metabolismo , Proteínas de Bactérias/metabolismo , Infecções por Helicobacter/microbiologia , Helicobacter pylori/metabolismo , Neoplasias Gástricas/microbiologia , Animais , Antígenos de Bactérias/genética , Proteínas da Membrana Bacteriana Externa/genética , Proteínas de Bactérias/genética , Transformação Celular Neoplásica/metabolismo , Transformação Celular Neoplásica/patologia , Transição Epitelial-Mesenquimal , Infecções por Helicobacter/complicações , Infecções por Helicobacter/diagnóstico , Infecções por Helicobacter/terapia , Helicobacter pylori/genética , Helicobacter pylori/patogenicidade , Interações Hospedeiro-Patógeno , Humanos , Proteínas Imediatamente Precoces/metabolismo , Fosfoproteínas/metabolismo , Proteínas de Ligação a RNA/metabolismo , Fatores de Risco , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Neoplasias Gástricas/prevenção & controle , Fator de Necrose Tumoral alfa/metabolismo , Proteínas Supressoras de Tumor/metabolismo
17.
Int J Mol Sci ; 22(7)2021 Mar 25.
Artigo em Inglês | MEDLINE | ID: mdl-33806236

RESUMO

Classic atherosclerosis risk factors do not explain all cases of chronic heart disease. There is significant evidence that gut microbiota may influence the development of atherosclerosis. The widespread prevalence of chronic Helicobacter pylori (H. pylori, HP) infections suggests that HP can be the source of components that stimulate local and systemic inflammatory responses. Elevated production of reactive oxygen species during HP infection leads to cholesterol oxidation, which drives atherogenesis. The aim of this study is to explore the link between persistent HP infection and a high-fat diet in the development of proinflammatory conditions that are potentially proatherogenic. An in vivo model of Caviae porcellus infected with HP and exposed to an experimental diet was investigated for the occurrence of a proinflammatory and proatherogenic endothelial environment. Vascular endothelial primary cells exposed to HP components were tested in vitro for oxidative stress, cell activation and apoptosis. The infiltration of inflammatory cells into the vascular endothelium of animals infected with HP and exposed to a high-fat diet was observed in conjunction with an increased level of inflammatory markers systemically. The arteries of such animals were the least elastic, suggesting the role of HP in arterial stiffness. Soluble HP components induced transformation of macrophages to foam cells in vitro and influenced the endothelial life span, which was correlated with Collagen I upregulation. These preliminary results support the hypothesis that HP antigens act synergistically with a high-fat diet in the development of proatherogenic conditions.


Assuntos
Dieta Aterogênica , Dieta Hiperlipídica , Endotélio Vascular/metabolismo , Infecções por Helicobacter/complicações , Animais , Anticorpos Antibacterianos/imunologia , Aterosclerose/etiologia , Aterosclerose/microbiologia , Modelos Animais de Doenças , Células Endoteliais/microbiologia , Feminino , Células Espumosas/metabolismo , Células Espumosas/microbiologia , Gastrite/metabolismo , Gastrite/microbiologia , Cobaias , Helicobacter pylori , Células Endoteliais da Veia Umbilical Humana , Humanos , Imunoglobulina G , Inflamação , Macrófagos/metabolismo , Macrófagos/microbiologia , Masculino , Rigidez Vascular
18.
Arq Gastroenterol ; 58(1): 114-119, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33909789

RESUMO

Helicobacter pylori is the main etiological agent of all malignant tumors caused by an infectious disease. It is a major, at times dominant, factor in the pathogenesis of a large spectrum of diseases such as acute and chronic gastritis, gastric and duodenal ulcers, gastric carcinoma, and lymphoma. Epidemiological and experimental studies suggest that H. pylori chronic infection may be related to different extragastric diseases, including colorectal neoplasms. This concise review aims to explore the association of H. pylori infection with colorectal cancer and adenoma, including the recent epidemiological findings, the diagnostic methods employed to detect H. pylori and virulent factors, and the potentially involved mechanisms. Furthermore, is attempted to establish the current data integration for causal inference using the Bradford-Hill causality criteria. The weak, although global, strength of the epidemiological positive association between H. pylori infection and colonic neoplasms associated to new mechanisms postulated to explain this interaction, including intestinal dysbiosis, should stimulate future studies. Prospective confirmatory studies to establish the role of H. pylori eradication in the process of carcinogenic transformation of the colonic epithelium may define its eventual role in the treatment and prevention of colonic neoplasms.


Assuntos
Neoplasias Colorretais , Gastrite , Infecções por Helicobacter , Helicobacter pylori , Neoplasias Gástricas , Neoplasias Colorretais/epidemiologia , Neoplasias Colorretais/etiologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/epidemiologia , Humanos , Estudos Prospectivos , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/etiologia
19.
Molecules ; 26(6)2021 Mar 12.
Artigo em Inglês | MEDLINE | ID: mdl-33809289

RESUMO

Matrix metalloproteinases (MMPs), key molecules of cancer invasion and metastasis, degrade the extracellular matrix and cell-cell adhesion molecules. MMP-10 plays a crucial role in Helicobacter pylori-induced cell-invasion. The mitogen-activated protein kinase (MAPK) signaling pathway, which activates activator protein-1 (AP-1), is known to mediate MMP expression. Infection with H. pylori, a Gram-negative bacterium, is associated with gastric cancer development. A toxic factor induced by H. pylori infection is reactive oxygen species (ROS), which activate MAPK signaling in gastric epithelial cells. Peroxisome proliferator-activated receptor γ (PPAR-γ) mediates the expression of antioxidant enzymes including catalase. ß-Carotene, a red-orange pigment, exerts antioxidant and anti-inflammatory properties. We aimed to investigate whether ß-carotene inhibits H. pylori-induced MMP expression and cell invasion in gastric epithelial AGS (gastric adenocarcinoma) cells. We found that H. pylori induced MMP-10 expression and increased cell invasion via the activation of MAPKs and AP-1 in gastric epithelial cells. Specific inhibitors of MAPKs suppressed H. pylori-induced MMP-10 expression, suggesting that H. pylori induces MMP-10 expression through MAPKs. ß-Carotene inhibited the H. pylori-induced activation of MAPKs and AP-1, expression of MMP-10, and cell invasion. Additionally, it promoted the expression of PPAR-γ and catalase, which reduced ROS levels in H. pylori-infected cells. In conclusion, ß-carotene exerts an inhibitory effect on MAPK-mediated MMP-10 expression and cell invasion by increasing PPAR-γ-mediated catalase expression and reducing ROS levels in H. pylori-infected gastric epithelial cells.


Assuntos
Mucosa Gástrica/efeitos dos fármacos , Helicobacter pylori/patogenicidade , Metaloproteinase 10 da Matriz/metabolismo , Inibidores de Metaloproteinases de Matriz/farmacologia , beta Caroteno/farmacologia , Catalase/metabolismo , Linhagem Celular , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/enzimologia , Células Epiteliais/microbiologia , Mucosa Gástrica/enzimologia , Mucosa Gástrica/microbiologia , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Infecções por Helicobacter/complicações , Infecções por Helicobacter/enzimologia , Infecções por Helicobacter/patologia , Helicobacter pylori/efeitos dos fármacos , Humanos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Metaloproteinase 10 da Matriz/genética , Invasividade Neoplásica/patologia , Invasividade Neoplásica/prevenção & controle , PPAR gama/metabolismo , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Neoplasias Gástricas/enzimologia , Neoplasias Gástricas/etiologia , Neoplasias Gástricas/patologia , Fator de Transcrição AP-1/metabolismo
20.
J Cancer Res Clin Oncol ; 147(6): 1685-1697, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-33738544

RESUMO

BACKGROUND/AIMS: A proliferation-inducing ligand (APRIL, also known as TNFSF13, CD256) is a member of the tumor necrosis factor (TNF) superfamily and involved in a diverse set of diseases. In this work, we explored the potential associations and underlying mechanism in patients suffered from gastric cancer between the expression of APRIL and H. pylori infection. METHODS: We analyzed APRIL expression levels in 200 GC tissue samples by immunohistochemistry staining. H. pylori infection was detected by modified Giemsa staining. The biological effects of APRIL on human GC cells in vitro and in vivo were tested by CCK-8 assay, colony formation, flow cytometry detection, transwell migration assay, matrigel invasion assay, and tumor xenograft assay in animals. RESULTS: APRIL reactivity was positively correlated with H. pylori infection in vitro and vivo. It turned out that the decrease of miR-145 expression was dose-dependent and time-dependent on H. pylori infection and in consistent with APRIL expression. MiR-145 significantly attenuated the effect of H. pylori infection on APRIL gene expression in SGC7901 and BGC823 cell lines. Furthermore, APRIL overexpression promoted the proliferation, migration, invasion, and transfer of GC cells and decreased apoptosis, while APRIL knockdown suppressed these effects. We confirmed that APRIL activated the canonical NF-κB pathway through phosphorylation of AKT. CONCLUSION: The expression of APRIL, which promoted the proliferation, migration, invasion, viability, and metastasis of GC cells, was upregulated in human H. pylori-infected GC through miR-145. Besides, APRIL-induced gastric tumorigenicity via activating NF-κB pathway. These results may provide a framework for the deeper analysis of APRIL in GC risk and prognosis.


Assuntos
Adenocarcinoma/genética , Helicobacter pylori/fisiologia , Neoplasias Gástricas/genética , Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/fisiologia , Adenocarcinoma/patologia , Adenocarcinoma/virologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Transformação Celular Viral/genética , Feminino , Regulação Neoplásica da Expressão Gênica , Infecções por Helicobacter/complicações , Infecções por Helicobacter/genética , Humanos , Masculino , Pessoa de Meia-Idade , Neoplasias Gástricas/patologia , Neoplasias Gástricas/virologia , Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
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