https://doi.org/10.5812/jjm.5038

Helicobacter pylori’s Evasion of the Immune System Could Establish an Inflammatory Environment That Potentially Induces the Development of Coronary Artery Disease

authors:

avatar Saman Maleki Vareki 1 , avatar Sayyed Hamid Zarkesh-Esfahani 1 , * , avatar Mohaddeseh Behjati 2

Department of Biology, Faculty of Science, University of Isfahan, Isfahan, IR Iran
Cardiovascular Research Center, Isfahan cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, IR Iran
Jundishapur Journal of Microbiology: Vol.6, issue 3; e94136
published online: May 01, 2013
article type: Research Article
received: May 20, 2019
accepted: June 20, 2012

how to cite: Maleki Vareki S, Zarkesh-Esfahani S H, Behjati M. Helicobacter pylori’s Evasion of the Immune System Could Establish an Inflammatory Environment That Potentially Induces the Development of Coronary Artery Disease. Jundishapur J Microbiol. 2013;6(3):e94136. https://doi.org/10.5812/jjm.5038.

Abstract

Background: Helicobacter pylori is responsible for one of the most common human infections and is a major risk factor for stomach ulcer disease and gastric cancer. H. pylori infection has been reported to be associated with generation and development of coronary artery disease (CAD). Moreover, diabetic patients positive for H. pylori infection showed a higher prevalence of CAD compared to H. pylori-negative patients. The main association between H. pylori infection and CAD seems to be generation of chronic low-grade inflammation.
Objectives: The current study aimed toinvestigate H. pylori’s capability to induce low-grade inflammation in the host; therefore H. pylori was compared to E. coli in its ability to activate neutrophils. Furthermore, H. pylori’s capability to induce apoptosis in peripheral blood lymphocytes was studied.
Materials and Methods: Peripheral blood neutrophils were treated with bacterial cells and the expression of the integrin CD11b that is critical for neutrophils adhesion, migration, and immune functions was assessed by flow cytometry. Additionally, peripheral blood lymphocytes were treated with H. pylori or E. coli then bacterial-induced apoptosis was examined by Annexin-V and Propidium Iodide (PI) staining.
Results: The obtained data showed that CD11b expression on cells treated with H. pylori was significantly lower than cells treated with E. coli. Furthermore, H. pylori induced apoptosis in lymphocytes significantly more than E. coli. Conclusions: Diminished neutrophilic activation along with enhanced lymphocytic apoptosis could explain enhanced predisposition to CAD through induced chronic low-grade inflammation.

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References

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