Abstract
Summaryof 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. Immunogastroenterology 2013; 2:132-145
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
