The Role of Gastric Mucosal Immunity in Gastric Diseases

Gastric mucosa plays its immune function through innate and adaptive immunity by recruiting immune cells and releasing corresponding cytokines, which have an inseparable relationship with gastric diseases. Whether infective gastric diseases caused by Helicobacter pylori, Epstein-Barr virus or other microbe, noninfective gastric diseases, or gastric cancer, gastric mucosal immunity plays an important role in the occurrence and development of the disease. Understanding the unique immune-related tissue structure of the gastric mucosa and its role in immune responses can help prevent gastric diseases or treat them through immunotherapy. In this review, we summarize the basic feature of gastric mucosal immunity and its relationship with gastric diseases to track the latest progress of gastric mucosal immunity, update relevant knowledge and provide theoretical reference for the prevention and treatment of gastric diseases based on the gastric mucosal immunity.

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Helicobacter pylori and Epstein–Barr Virus Infection in Gastric Diseases: Correlation with IL-10 and IL1RN Polymorphism

Journal of Oncology ◽

10.1155/2019/1785132 ◽

2019 ◽

Vol 2019 ◽

pp. 1-8 ◽

Cited By ~ 7

Author(s):

Fasciana Teresa ◽

Nicola Serra ◽

Giuseppina Capra ◽

Chiara Mascarella ◽

Cesare Gagliardi ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Gastric Mucosa ◽

Chronic Gastritis ◽

Epstein Barr Virus ◽

Normal Gastric Mucosa ◽

Gastric Diseases ◽

Barr Virus ◽

Genes Encoding ◽

Epstein Barr

Introduction. Helicobacter pylori and Epstein–Barr virus (EBV) infection have recently been shown to be associated with gastric diseases. Polymorphisms in genes encoding cytokines such as interleukin 10 (IL-10) and interleukin 1 Receptor (IL-1RN) influence cytokine secretion levels and appear to contribute to the risk of developing gastroduodenal diseases. To our knowledge, this is the first preliminary study to address the association of coinfection with H. pylori and EBV and their correlation with genetic predisposition in the development of gastric diseases. Methods. Gastric biopsy samples of 96 patients with different gastric diseases were used. Results. Our results showed that the rate of coinfection was higher in patients with gastric cancer than in patients with normal gastric mucosa, active chronic gastritis, and MALT lymphoma. As regards the characterization of H. pilory strains, the polymorphism s1m1i1 of vacA gene was more frequent in patients with MALT Lymphoma in comparison to others, while the polymorphism s2m2i2 was most frequent in patients with normal gastric mucosa. In addition, patients who tested positive for the cagA gene were more frequently those affected with gastric cancer than those with inactive chronic gastritis. Similarly, the patients with oipA gene ON were more frequently those with gastric cancer than those with inactive chronic gastritis. Conclusion. According to our analysis, there was no correlation between coinfection and polymorphisms in genes encoding IL-10 and IL-1RN. We conclude that various factors can be involved in the development of gastric diseases.

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in vivo and in vitro analysis of the functional role of Epstein-Barr virus-induced gene 3 (EBI3) for regulation of Th2 mediated immune responses

Gastroenterology ◽

10.1016/s0016-5085(03)81688-8 ◽

2003 ◽

Vol 124 (4) ◽

pp. A335

Author(s):

Stefan J. Wirtz ◽

Christoph Becker ◽

Edward E.S. Nieuwenhuis ◽

Mark Birkenbach ◽

Richard S. Blumberg ◽

...

Keyword(s):

Immune Responses ◽

Functional Role ◽

Epstein Barr Virus ◽

Barr Virus ◽

Epstein Barr ◽

Vitro Analysis ◽

In Vitro Analysis

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Are Viruses and Parasites Linked to Celiac Disease? A Question that Still has no Definite Answer

Current Pharmaceutical Biotechnology ◽

10.2174/1389201020666190828124924 ◽

2019 ◽

Vol 20 (14) ◽

pp. 1181-1193 ◽

Cited By ~ 1

Author(s):

Aref Shariati ◽

Hamid R. Aslani ◽

Mohammad R.H. Shayesteh ◽

Ali Taghipour ◽

Ahmad Nasser ◽

...

Keyword(s):

Celiac Disease ◽

Multiple Roles ◽

Barr Virus ◽

The People ◽

Intestinal Infections ◽

Inflammatory Bowel ◽

Epstein Barr ◽

Irritable Bowel ◽

Related Proteins

Celiac Disease (CD) is a complex autoimmune enteropathy of the small intestine that commonly occurs in genetically predisposed individuals due to intake of gluten and related proteins. Gluten consumption, duration of breast-feeding, various infections, especially frequent intestinal infections, vaccinations and use of antibiotics can be linked to CD. It is predicted that it affects 1% of the global population and its incidence rate is increasing. Most of the people with the HLA-DQ2 or HLADQ8 are at a higher risk of developing this disease. The link between infections and autoimmune diseases has been very much considered in recent years. In several studies, we explained that pathogenic and non-pathogenic microorganisms might have multiple roles in initiation, exacerbation, and development of Irritable Bowel Syndrome (IBS) and Inflammatory Bowel Disease (IBD). In various studies, the relationship between infections caused by viruses, such as Epstein-Barr Virus (EBV), Rotavirus, Hepatitis C (HCV), Hepatitis B virus (HBV), Cytomegalovirus (CMV), and Influenza virus, and parasites including Giardia spp. and Toxoplasma gondii with CD has been raised. However, increasing evidence proposes that some of these microorganisms, especially helminths, can also have protective and even therapeutic roles in the CD process. Therefore, in order to determine the role of microorganisms in the process of this disease, we attempted to summarize the evidence suggesting the role of viral and parasitic agents in pathogenesis of CD.

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Role of surgery in treating epstein‐barr virus‐associated smooth muscle tumor (EBV‐SMT) with central nervous system invasion: A systemic review from 1997 to 2019

Cancer Medicine ◽

10.1002/cam4.3770 ◽

2021 ◽

Vol 10 (5) ◽

pp. 1473-1484

Author(s):

Ka‐Wei Lau ◽

Yu‐Wei Hsu ◽

Yin‐Ting Lin ◽

Ko‐Ting Chen

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Epstein Barr Virus ◽

Smooth Muscle Tumor ◽

Systemic Review ◽

Barr Virus ◽

Epstein Barr ◽

Central Nervous System Invasion ◽

Muscle Tumor

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Molecular Genetics in Epstein–Barr Virus-Associated Malignancies

Life ◽

10.3390/life11070593 ◽

2021 ◽

Vol 11 (7) ◽

pp. 593

Author(s):

Srikanth Umakanthan ◽

Maryann M Bukelo

Keyword(s):

Epstein Barr Virus ◽

Diagnostic Tools ◽

Main Role ◽

Genetic Changes ◽

Barr Virus ◽

Cancer Pathogenesis ◽

Genomic Studies ◽

Epstein Barr ◽

Oncogenic Form

Global genomic studies have detected the role of genomic alterations in the pathogenesis of Epstein–Barr virus (EBV)-associated tumors. EBV oncoproteins cause a vital shift of EBV from an infectious virus to an oncogenic form during the latent and lytic phase within the lymphoid B cells and epithelial cells. This epigenetic alteration modulates the virus and host genomes and inactivates and disrupts numerous tumor suppressors and signaling pathways. Genomic profiling has played the main role in identifying EBV cancer pathogenesis and its related targeted therapies. This article reviews the role of genetic changes in EBV-associated lymphomas and carcinomas. This includes the prolific molecular genesis, key diagnostic tools, and target-specific drugs that have been in recent clinical use.

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EBV load is associated with cfDNA fragmentation and renal damage in SLE patients

Lupus ◽

10.1177/09612033211010339 ◽

2021 ◽

pp. 096120332110103

Author(s):

Anna Truszewska ◽

Agnieszka Wirkowska ◽

Kamila Gala ◽

Piotr Truszewski ◽

Łucja Krzemień-Ojak ◽

...

Keyword(s):

Kidney Disease ◽

Lupus Erythematosus ◽

Epstein Barr Virus ◽

Renal Damage ◽

Healthy Individuals ◽

Pcr Assay ◽

Barr Virus ◽

Fragmentation Index ◽

Epstein Barr

Background For long Epstein–Barr virus (EBV) has been suspected to be involved in the pathogenesis of systemic lupus erythematosus (SLE). The aim of this study was to verify the association between EBV, cell-free DNA (cfDNA) and kidney disease in SLE. Methods Blood samples were obtained from 43 SLE patients and 50 healthy individuals. EBV load was measured via real-time PCR assay. Sizing and quantification of plasma cfDNA was performed on Bioanalyzer. We proposed that the uniformity of cfDNA fragmentation can be described using cfDNA fragmentation index. Results SLE patients with chronic kidney disease (CKD +) had higher EBV load compared to CKD(–) patients (P = 0.042). Patients with high cfDNA level had higher EBV load (P = 0.041) and higher cfDNA fragmentation index (P < 0.001) compared to patients with low cfDNA level. Among patients with high cfDNA level, EBV load was higher in CKD(+) group compared to CKD(–) group (P = 0.035). EBV load was positively correlated with the fragmentation index in all SLE patients (P = 0.028, R2 = 0.13), and the correlation was even more pronounced in CKD (+) patients (P < 0.001, R2 = 0.20). Conclusions We showed that EBV load was associated with non-uniform cfDNA fragmentation, higher cfDNA levels, and kidney disease in SLE patients. Although the causality of this relationship could not be determined with the current study, it brings rationale for further investigations on the role of EBV and cfDNA interplay in SLE pathogenesis.

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Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Human Herpesviruses Are Back!

Biomolecules ◽

10.3390/biom11020185 ◽

2021 ◽

Vol 11 (2) ◽

pp. 185

Author(s):

Maria Eugenia Ariza

Keyword(s):

Chronic Fatigue Syndrome ◽

Disease Process ◽

Chronic Fatigue ◽

Myalgic Encephalomyelitis ◽

Barr Virus ◽

Fatigue Syndrome ◽

Specific Proteins ◽

Epstein Barr ◽

Human Herpesviruses

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) or Systemic Exertion Intolerance Disease (SEID) is a chronic multisystem illness of unconfirmed etiology. There are currently no biomarkers and/or signatures available to assist in the diagnosis of the syndrome and while numerous mechanisms have been hypothesized to explain the pathology of ME/CFS, the triggers and/or drivers remain unknown. Initial studies suggested a potential role of the human herpesviruses especially Epstein-Barr virus (EBV) in the disease process but inconsistent and conflicting data led to the erroneous suggestion that these viruses had no role in the syndrome. New studies using more advanced approaches have now demonstrated that specific proteins encoded by EBV could contribute to the immune and neurological abnormalities exhibited by a subgroup of patients with ME/CFS. Elucidating the role of these herpesvirus proteins in ME/CFS may lead to the identification of specific biomarkers and the development of novel therapeutics.

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