scholarly journals Chemokines in the gastric mucosa in Helicobacter pylori infection

Gut ◽  
1998 ◽  
Vol 42 (5) ◽  
pp. 609-617 ◽  
Author(s):  
Y Yamaoka ◽  
M Kita ◽  
T Kodama ◽  
N Sawai ◽  
T Tanahashi ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Expression Patterns ◽  
Enzyme Linked Immunosorbent Assay ◽  
Biopsy Specimens ◽  
Inflammatory Protein ◽  
Polymerase Chain ◽  
H Pylori ◽  
Macrophage Inflammatory Protein

Background—Although chemokines have been suggested to play an important role in Helicobacter pyloriassociated gastritis, few studies have investigated the role of chemokines other than interleukin 8 (IL-8) in gastric mucosa.Aims—To investigate the expression and production patterns of various chemokines using gastric biopsy specimens.Methods—In 192 patients, expression patterns of C-X-C chemokines (IL-8 and growth regulated α (GROα)) and C-C chemokines (regulated on activation, normal T cell expressed and presumably secreted (RANTES), monocyte chemotactic and activating factor (MCAF), macrophage inflammatory protein 1α (MIP-1α), and MIP-1β) were examined using reverse transcription polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assay (ELISA).cagA gene was identified using PCR.Results—H pylori infection was associated with increased rates of expression of mRNA for IL-8, GROα, RANTES, and MIP-1α and with increased levels of mucosal IL-8 and GROα. IL-8 and GROα levels correlated with the density of H pylori in both the antrum and corpus. The levels of these chemokines correlated with cellular infiltration in the antrum but not the corpus. cagA gene positive H pyloriinfection was associated with increased rates of expression of mRNA for IL-8 and GROα and with increased levels of these chemokines.Conclusion—H pylori infection is associated with increased expression rates and production of C-X-C chemokines (IL-8 and GROα), but not with increased production of C-C chemokines. Although H pylori infection is associated with increased C-X-C chemokines in the antrum and corpus, there is a difference in the inflammatory response between these two areas of the stomach.

scholarly journals Induction of various cytokines and development of severe mucosal inflammation by cagA gene positive Helicobacter pylori strains

Gut ◽  
1997 ◽  
Vol 41 (4) ◽  
pp. 442-451 ◽  
Author(s):  
Y Yamaoka ◽  
M Kita ◽  
T Kodama ◽  
N Sawai ◽  
K Kashima ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Expression Patterns ◽  
Mucosal Inflammation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Biopsy Specimens ◽  
Tnf Α ◽  
Polymerase Chain ◽  
H Pylori ◽  
Factor Α ◽  
Necrosis Factor

Background—Helicobacter pyloristrains possessing the cagA gene are thought to induce interleukin 8 (IL-8) in gastric mucosa. However, it is still unclear whether a relation exists between the cagA gene and the expression patterns of cytokines other than IL-8.Aims—To investigate the relation between the cagA gene and the production of various cytokine proteins using an enzyme linked immunosorbent assay (ELISA).Patients and methods—In 184 patients, the cagA gene was detected by polymerase chain reaction (PCR), and levels of production of IL-1β, IL-6, IL-7, IL-8, IL-10, and tumour necrosis factor α (TNF-α) in antral biopsy specimens were measured by ELISA.Results—Mucosal levels of IL-1β, IL-6, IL-8, and TNF-α were significantly higher in H pyloripositive than in H pylori negative patients. Furthermore, the mucosal levels of IL-1β and IL-8 were significantly higher in specimens infected with cagApositive strains than in those infected with cagAnegative strains. In H pylori positive patients, the mucosal level of IL-8 was closely correlated with that of IL-1β (p<0.0001), and the mucosal level of IL-6 was closely correlated with that of TNF-α (p<0.0001).Conclusion—These findings suggest that the ability to induce cytokines differs among the strains;cagA+ strains induce various kinds of cytokines and may cause severe inflammation, whereascagA− strains induce IL-8 and IL-1β only weakly and may cause only mild inflammation. However, as most patients infected with the cagA+ strains have gastritis, these strains may not be equivalent to ulcerogenic strains.

scholarly journals Interleukin-17C in Human Helicobacter pylori Gastritis

2017 ◽  
Vol 85 (10) ◽  
Author(s):  
Shingo Tanaka ◽  
Hiroyuki Nagashima ◽  
Modesto Cruz ◽  
Tomohisa Uchida ◽  
Takahiro Uotani ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Gastric Biopsy ◽  
Interleukin 17 ◽  
Human Gastric Mucosa ◽  
Mrna Levels ◽  
Content Type ◽  
Biopsy Specimens ◽  
H Pylori

ABSTRACT The interleukin-17 (IL-17) family of cytokines (IL-17A to IL-17F) is involved in many inflammatory diseases. Although IL-17A is recognized as being involved in the pathophysiology of Helicobacter pylori-associated diseases, the role of other IL-17 cytokine family members remains unclear. Microarray analysis of IL-17 family cytokines was performed in H. pylori-infected and uninfected gastric biopsy specimens. IL-17C mRNA was upregulated approximately 4.5-fold in H. pylori-infected gastric biopsy specimens. This was confirmed by quantitative reverse transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominican Republic. Immunohistochemical analysis showed that IL-17C expression in H. pylori-infected gastric biopsy specimens was predominantly localized to epithelial and chromogranin A-positive endocrine cells. IL-17C mRNA levels were also significantly greater among cagA-positive than cagA-negative H. pylori infections (P = 0.012). In vitro studies confirmed an increase in IL-17C mRNA and protein levels in cells infected with cagA-positive infections compared to cells infected with either cagA-negative or cag pathogenicity island (PAI) mutant. Chemical inhibition of IκB kinase (IKK), mitogen-activated protein extracellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17C proteins in infected cells, whereas p38 inhibition had no effect on IL-17C protein secretion. In conclusion, H. pylori infection was associated with a significant increase in IL-17C expression in human gastric mucosa. The role of IL-17C in the pathogenesis of H. pylori-induced diseases remains to be determined.

scholarly journals Helicobacter pylori Recombinant CagA Regulates Th1/Th2 Balance in a BALB/c Murine Model

2020 ◽  
Vol 10 (2) ◽  
pp. 264-270
Author(s):  
Nafiseh Paydarnia ◽  
Behzad Mansoori ◽  
Davoud Esmaeili ◽  
Tohid Kazemi ◽  
Mahyar Aghapour ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Chain Reaction ◽  
Protein Levels ◽  
Cytotoxin Associated Gene A ◽  
Polymerase Chain ◽  
H Pylori ◽  
Antibody Levels

Purpose: Helicobacter pylori is recognized as one of the prevalent causes of human gastricinfection. In the present study, the role of mixed immunization with H. pylori lipopolysaccharide(LPS) and recombinant cytotoxin-associated gene A (rCagA) as a stimulator of host immuneresponses was determined. Methods: BALB/c mice were immunized with different formulations by the systemic administrationat 14-day intervals. The effects of the formulations plus CpG adjuvants were assessed before andpost-immunization in separated studies. Moreover, the expression of Th1/Th2 cytokines wasquantified in sera of immunized mice using reverse transcription polymerase chain reaction (RTPCR)test and the protein levels confirmed with enzyme linked immunosorbent assay (ELISA).Finally, the specific antibody levels in sera were studied by ELISA and the tendency of cellularresponse was examined by IgG1/IgG2a ratio. Results: Data of Western blotting verified the presence of constructed protein. Analysisof lymphocyte proliferation showed that CpG-conjugated rCagA increases lymphocytesproliferation compared to the control group. Also, it was shown that formulations containing LPSand rCagA promote a Th1 response indicated by interferon-gamma expression and induced Th1/Th2 balance. Additionally, the specific IgG1, total IgG and IgG2a levels elevated in response toall treatments. Ultimately, the IgG2a/IgG1 ratio in the mice immunized with rCagA-containingformulations increased. Conclusion: These results indicated that rCagA protein carried with CpG adjuvant not onlymaintained its antigenicity throughout the experiment but also induced robust Th1-biasedimmune responses. Therefore, it holds promise for the production of an efficient vaccine againstH. pylori infection. <br />

scholarly journals Helicobacter pylori infection reduces the risk of gastroesophageal reflux disease

2021 ◽  
pp. 96-101
Author(s):  
R. I. Khlynova ◽  
O. M. Khromtsova ◽  
R. B. Berdnikov ◽  
I. B. Khlynov
Keyword(s):  
Helicobacter Pylori ◽  
Gastroesophageal Reflux Disease ◽  
Gastric Mucosa ◽  
Gastroesophageal Reflux ◽  
Observational Study ◽  
Reflux Disease ◽  
Helicobacter Pylori Infection ◽  
Cross Sectional ◽  
Biopsy Specimens ◽  
H Pylori

The aim is to study the effect of Helicobacter pylori infection on risk of developing gastroesophageal reflux disease. Materials and methods - cross-sectional observational study of 1007 patients with dyspepsia syndrome who underwent videoesophagogastroduodenoscopy with biopsy and histological examination of biopsy specimens of the gastric mucosa by OLGA-system. The age, gender, overweight, cigarette smoking, presence of Helicobacter pylori infection and gastritis stage were assessed. Results - the study showed a significant decrease in the incidence of gastroesophageal reflux disease in patients with positive H. Pylori status by 4% (RR 0,68; 95% CI, 0.49-0.94, p=0,041). The risk of developing gastroesophageal reflux disease significantly higher in overweight (RR 2,62; 95% CI 2,0-3,56; р<0,001) men (RR 1,76; 95% CI 1,33-2,32; р=0,0046) who smoked cigarettes (RR 3,23; 95% CI 2,45-4,24; р<0,001) and was not associated with the patient’s age and the stage of gastritis (р>0,05). Conclusion - a significant reduction in the frequency and risk of developing gastroesophageal reflux disease in patients with Helicobacter pylori infection is demonstrated.

scholarly journals Role of Gamma Interferon in Helicobacter pylori Induction of Inflammatory Mediators during Murine Infection

2002 ◽  
Vol 70 (6) ◽  
pp. 3295-3299 ◽  
Author(s):  
Marygorret Obonyo ◽  
Donald G. Guiney ◽  
Julia Harwood ◽  
Joshua Fierer ◽  
Sheri P. Cole
Keyword(s):  
Helicobacter Pylori ◽  
Gene Knockout ◽  
Gamma Interferon ◽  
Epithelial Cell Line ◽  
Inos Mrna ◽  
Inflammatory Protein ◽  
Ifn Γ ◽  
H Pylori ◽  
Oxide Synthase

ABSTRACT Gamma interferon (IFN-γ) has been proposed to play an important role in Helicobacter-related gastritis. Using the IFN-γ gene knockout (IFN-γ−/−) mouse model and a murine gastric epithelial cell line, GSM06, we demonstrated that Helicobacter pylori maximally induced macrophage inflammatory protein-2 (MIP-2) and inducible nitric oxide synthase (iNOS) mRNA only in wild-type mice. MIP-2 and iNOS mRNA were also induced by H. pylori in GSM06 cells. Induction of cyclooxygenase 2 mRNA through IFN-γ was demonstrated in GSM06 cells. These data indicate that IFN-γ mediates the induction of MIP-2 and iNOS mRNA expression by H. pylori in mice.

scholarly journals Potential Role of the Chemokine Macrophage Inflammatory Protein 1α in Human and Experimental Schistosomiasis

2005 ◽  
Vol 73 (4) ◽  
pp. 2515-2523 ◽  
Author(s):  
Adriano L. S. Souza ◽  
Ester Roffê ◽  
Vanessa Pinho ◽  
Danielle G. Souza ◽  
Adriana F. Silva ◽  
...  
Keyword(s):  
Potential Role ◽  
Severe Disease ◽  
Experimental Studies ◽  
Interleukin 4 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein ◽  
Deficient Mice

ABSTRACT In human schistosomiasis, the concentrations of the chemokine macrophage inflammatory protein 1α (MIP-1α/CCL3) is greater in the plasma of patients with clinical hepatosplenic disease. The objective of the present study was to confirm the ability of CCL3 to detect severe disease in patients classified by ultrasonography (US) and to evaluate the potential role of CCL3 in Schistosoma mansoni-infected mice. CCL3 was measured by enzyme-linked immunosorbent assay in the plasma of S. mansoni-infected patients. CCL3-deficient mice were infected with 25 cercariae, and various inflammatory and infectious indices were evaluated. The concentration of CCL3 was higher in the plasma of S. mansoni-infected than noninfected patients. Moreover, CCL3 was greater in those with US-defined hepatosplenic than with the intestinal form of the disease. In CCL3-deficient mice, the size of the granuloma and the liver eosinophil peroxidase activity and collagen content were diminished compared to wild-type mice. In CCL3-deficient mice, the worm burden after 14 weeks of infection, but not after 9 weeks, was consistently smaller. The in vitro response of mesenteric lymph node cells to antigen stimulation was characterized by lower levels of interleukin-4 (IL-4) and IL-10. CCL3 is a marker of disease severity in infected humans, and experimental studies in mice suggest that CCL3 may be a causative factor in the development of severe schistosomiasis.

H. pylori and transient lower esophageal sphincter relaxations induced by gastric distension in healthy humans

2001 ◽  
Vol 281 (2) ◽  
pp. G350-G356 ◽  
Author(s):  
Frank Zerbib ◽  
Valérie Bicheler ◽  
Véronique Leray ◽  
Madeleine Joubert ◽  
Stanislas Bruley des Varannes ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Lower Esophageal Sphincter ◽  
Proinflammatory Cytokine ◽  
Healthy Subjects ◽  
Gastric Distension ◽  
Healthy Humans ◽  
Biopsy Specimens ◽  
Esophageal Sphincter ◽  
H Pylori

The role of Helicobacter pylori infection in the control of lower esophageal sphincter (LES) motility, especially the occurrence of transient LES relaxations (TLESRs), was studied in eight H. pylori-positive and eight H. pylori-negative healthy subjects. During endoscopy, biopsy specimens were taken from the cardia, fundus, and antrum for determinations of H. pyloristatus, gastritis, and proinflammatory cytokine mucosal concentrations. LES motility was monitored during three different 30-min periods: baseline, gastric distension (barostat), and gastric distension with CCK infusion. Gastric distension significantly increased the TLESR rate, whereas CCK increased the rate of distension-induced TLESRs further and reduced resting LES pressure without significant differences between infected and noninfected subjects. H. pylori status did not influence resting LES pressure or gastric compliance. Cytokine mucosal concentrations were increased in infected patients, but no correlation was found with the TLESR rate, which was also independent of inflammation at the cardia, fundus, and antrum. These results suggest that H. pylori-associated inflammation does not affect the motor events involved in the pathogenesis of gastroesophageal reflux.

scholarly journals Relationship of Anti-Lewis x and Anti-Lewis y Antibodies in Serum Samples from Gastric Cancer and Chronic Gastritis Patients toHelicobacter pylori-Mediated Autoimmunity

2001 ◽  
Vol 69 (8) ◽  
pp. 4774-4781 ◽  
Author(s):  
Michael A. Heneghan ◽  
Ciaran F. McCarthy ◽  
Daiva Janulaityte ◽  
Anthony P. Moran
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Antibody Production ◽  
Enzyme Linked Immunosorbent Assay ◽  
Serum Samples ◽  
Lewis Y ◽  
H Pylori ◽  
Negative Controls ◽  
Relationship Of

ABSTRACT Lewis (Le) antigens have been implicated in the pathogenesis of atrophic gastritis and gastric cancer in the setting ofHelicobacter pylori infection, and H. pylori-induced anti-Le antibodies have been described that cross-react with the gastric mucosa of both mice and humans. The aim of this study was to examine the presence of anti-Le antibodies in patients with H. pylori infection and gastric cancer and to examine the relationships between anti-Le antibody production, bacterial Le expression, gastric histopathology, and host Le erythrocyte phenotype. Anti-Le antibody production and H. pylori Le expression were determined by enzyme-linked immunosorbent assay, erythrocyte Le phenotype was examined by agglutination assays, and histology was scored blindly. Significant levels of anti-Lex antibody (P < 0.0001, T = 76.4, DF = 5) and anti-Ley antibody (P < 0.0001, T = 73.05, DF = 5) were found in the sera of patients with gastric cancer and other H. pylori-associated pathology compared with H. pylori-negative controls. Following incubation of patient sera with synthetic Le glycoconjugates, anti-Lex and -Ley autoantibody binding was abolished. The degree of the anti-Lex and -Leyantibody response was unrelated to the host Le phenotype but was significantly associated with the bacterial expression of Lex (r = 0.863,r 2 = 0.745, P < 0.0001) and Ley (r = 0.796,r 2 = 0.634, P < 0.0001), respectively. Collectively, these data suggest that anti-Le antibodies are present in most patients with H. pyloriinfection, including those with gastric cancer, that variability exists in the strength of the anti-Le response, and that this response is independent of the host Le phenotype but related to the bacterial Le phenotype.

scholarly journals Relationship Between Mucosal TNF-α Expression and Th1, Th17, Th22 and Treg Responses in Helicobacter Pylori Infection

2021 ◽  
Author(s):  
Ghorbanali Rahimian ◽  
Milad Shahini Shams Abadi ◽  
Reza Ahmadi ◽  
Mohammedhadi Shafigh ◽  
Fatemeh Azadegan-Dehkordi
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Treg Cells ◽  
Infected Group ◽  
Ulcer Disease ◽  
Tnf Α ◽  
H Pylori ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background: Helicobacter pylori (H. pylori) -induced gastric inflammation in the gastric mucosa and significantly increases the risk of developing gastritis and peptic ulcer disease (PUD). The objective of this research is to determine the role of tumor necrosis factor-α (TNF-α) expression in the gastric mucosa of patients with H. pylori –associated gastritis and PUD compared to uninfected patients, and we determined the relation between TNF-α expression and Th1/Th17/Th22, and Treg cells.Methods: Fifty-five patients with H. pylori –associated gastritis, 47 patients with H. pylori –associated PUD, and 48 uninfected patients were in this research. Antrum biopsy was used to detect H. pylori, virulence factors and histopathological assessments.Results: Expression of TNF-α in the infected group was significantly higher than the uninfected group. Also, cagA/oipA-positive infected patients induce significantly more TNF-α expression than do cagA/oipA-negative infected patients. Expression of TNF-α was significantly increased in the PUD group than the gastritis group. Notably, TNF-α expression had a significant positive correlation with the frequency of Th1/Th17/Th22 lymphocytes in the PUD group.Conclusion: These findings indicate the importance of increasing TNF-α with Th1, Th17, Th22 responses increase as an important risk factor for PUD in context of H. pylori infection.

scholarly journals Helicobacter pylori infection and inflammatory bowel diseases

2021 ◽  
Vol 11 (1) ◽  
pp. 68-78
Author(s):  
Yu. P. Uspenskiy ◽  
N. V. Baryshnikova ◽  
A. N. Suvorov ◽  
A. V. Svarval
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Inflammatory Bowel Diseases ◽  
Pathogenic Bacteria ◽  
T Cell Response ◽  
Aminosalicylic Acid ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
H Pylori

Helicobacter pylori is detected in the human intestine on average in 35% of clinical cases, but the question about its etiopathogenetic role in intestinal diseases has not been fully investigated. Many scientists study a relationship between the H. pylori persistence and development of various bowel diseases. Diverse viewpoints have been proposed regarding a potential link between H. pylori and inflammatory bowel diseases (IBD). Here we review the data from domestic and foreign studies aimed at examining potential role of H. pylori both as a trigger and protector resulting in the pathogenetic alterations leading to developing Crohn‘s disease and ulcerative colitis. The former is favored by the hypothesis wherein H. pylori may trigger IBD due to potential connection between extragastric infection and its direct damaging action as well as indirect effects contributing to the initiation of oxidative stress, autoimmune aggression and development of intestinal dysbiosis. In addition, the effects of enterohepatic Helicobacter spp. promoting IBD pathogenesis are discussed. The mechanisms underlying the protective role of H. pylori infection may be driven via differentially expressed acute and/or chronic local inflammatory mucosal response able to downmodulate systemic immune responses and suppress autoimmune reactions, as well as skewing host immune response from a pro-inflammatory Th1/Th17 cell-mediated towards regulatory T-cell response. Moreover, it was found that H. pylori may induce production of antibacterial peptides counteracting potentially pathogenic bacteria involved in IBD pathogenesis. In particular, it was found that IBD patients are dominated with moderate active antral gastritis coupled to atrophy, with the peak intensity observed in patients under 30 years of age. Intensity of intestinal metaplasia in the gastric mucosa of IBD patients accounted for by the duration of the disease course. Basal IBD therapy with 5-aminosalicylic acid lowers severity and activity of gastritis, degree of atrophy as well as magnitude H. pylori invasion in the gastric mucosa. There is evidence that 5-aminosalicylic acid-containing drugs may result in a so-called “spontaneous eradication” of H. pylori infection. Extended investigations are required to examine a role of H. pylori in IBD pathogenesis.

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