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Jul/Aug/Sep 2013; 2(3)

Autophagy in Helicobacter pylori-Induced Inflammation and Disease

Evangelos Kazakos, Nick Dorrell, Jannis Kountouras

+Author Affiliations

Evangelos Kazakos

Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece

Nick Dorrell

Department of Pathogen Molecular Biology, Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, UK

Jannis Kountouras

Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece

Corresponding Author:

Evangelos Kazakos, ekazakos@gmail.com

Abstract

Co-adaptation of Helicobacter pylori (Hp) with its human host requires the bacterium’s ingenious ability to orchestrate epithelial cell signaling to maintain a state of mucosal immune activation ultimately, dictating infection outcomes. Autophagy has been intimately involved in tailoring the inflammatory response upon intracellular sensing of bacterial constituents. Highly adapted microorganisms have evolved strategies to subvert autophagy by persisting inside autophagosomes whereas, loss of autophagy delays global turnover of ubiquitylated cargos leading to the accumulation of misfolded proteins and p62/SQSTM1 and NBR1 complexes linked to tumorigenesis. Genome-wide association screens have identified the existence of genetic predisposition loci related to polymorphisms affecting the autophagic modulator ATG16L1 and the autophagy-related factor IRGM. The present review aims at: i. presenting recent advances regarding the role of autophagy in the pathophysiology of Hp infection; and ii. offering possible projections of data related to other pathogens in the context of studying Hp-induced pathologies, aiding future research.

Received May 9, 2013.

Revised June 16, 2013.

Accepted June 17, 2013.

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Published September 20, 2013;

DOI:10.7178/ig.41

Immunogastroenterology

2013;2(3): 132-145.

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