Autophagy and Burkholderia

Abstract

Autophagy has become increasingly viewed as an important component of the eukaryotic innate immune system. The elimination of intracellular pathogens by autophagy in mammalian cells (xenophagy) results not only in the degradation of invading bacteria, viruses, fungi and parasites, but also liberation of metabolites that may have been utilized during pathogen infection, thus promoting cell survival. After gaining entry into the cell, intracellular bacterial pathogens attempt to escape from phagosomes (or endosomes) into the cytosol where they endeavour to continue the infection cycle unhindered by host cell protective mechanisms. Bacterial recognition resulting from either their cytosolic location, the secretion of bacterial products, or phagosomal membrane damage, can induce autophagy. In this context, induction of autophagy results in the clearance of some bacterial pathogens, whereas other bacteria are able to manipulate autophagy for their own benefit and appear to effectively replicate within autophagosome-like vesicles. Some bacteria are seemingly able to evade autophagy and Burkholderia pseudomallei is one of them. This review will discuss the autophagic processes that may be activated by host cells to provide protection against infection by this bacterial pathogen.

Metformin induced autophagy in diabetes mellitus – Tuberculosis co-infection patients: A case study

“…Several studies related to the autophagy in TB infection, suggest that SOD and IFN-g play important role in autophagy 21,25,31,32 and the results of this study support those information.…”

Hepatitis B virus dampens autophagy maturation via negative regulation of Rab7 expression

“…Autophagy, a conserved cellular protective mechanism, has been regarded as a key component of the innate immune system (21). Induction of autophagy results in the elimination of invading pathogens, whereas some microbes have evolved strategies to manipulate autophagy for their own benefit.…”

Evolution ofbopAGene inBurkholderia: A Case of Convergent Evolution as a Mechanism for Bacterial Autophagy Evasion

“…The Shigella IcsB protein interferes with autophagy systems by binding to the Shigella surface protein IcsA, thereby competitively inhibiting binding of the autophagy protein Atg5 to IcsA. Although the mechanism(s) by which B. pseudomallei evade autophagy remains unknown, it is unlikely that BopA acts in a manner analogous to IcsB which facilitates bacterial evasion of autophagy [16, 17]. When the sequence identity falls within or below the twilight zone of 20–25%, the evolutionary relatedness of proteins cannot be assumed [18].…”