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

How to Cite:Saman Maleki VarekiSayyed Hamid Zarkesh-EsfahaniMohaddeseh BehjatiHelicobacter pylori’s Evasion of the Immune System Could Establish an Inflammatory Environment That Potentially Induces the Development of Coronary Artery Disease.Jundishapur J Microbiol.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.

Keywords

Fulltext

Fulltext is available in pdf file.

References

1.
The references are available in PDF file.

comments

Crossmark

Checking

Share on

Comments

Number of Comments:0

Cited by

Metrics

Get Permission (article level)

Purchasing Reprints

Copyright Clearance Center (CCC) handles bulk orders for article reprints for Brieflands. To place an order for reprints, please click here ( https://www.copyright.com/landing/reprintsinquiryform/ ). Clicking this link will bring you to a CCC request form where you can provide the details of your order. Once complete, please click the ‘Submit Request’ button and CCC’s Reprints Services team will generate a quote for your review.

Search Relations

Author(s):

Saman Maleki Vareki:[PubMed][Scholar]
Sayyed Hamid Zarkesh-Esfahani:[PubMed][Scholar]
Mohaddeseh Behjati:[PubMed][Scholar]