title: 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.
authors.affiliation: Department of Biochemistry and Molecular Biology, Monash University, Clayton Campus, Melbourne, VIC, Australia.
authors.forename: Rodney J
authors.identifier: 0000000169778281
authors.initials: RJ
authors.lastname: Devenish
authors.affiliation: Department of Biochemistry and Molecular Biology, Monash University, Clayton Campus, Melbourne, VIC, Australia.
authors.forename: Shu-chin
authors.initials: SC
authors.lastname: Lai
mesh_terms: D001343:Autophagy / Q000235:genetics / Q000276:immunology*; D001426:Bacterial Proteins / Q000235:genetics / Q000276:immunology*; D016957:Burkholderia pseudomallei / Q000276:immunology*; D005786:Gene Expression Regulation; D054884:Host-Pathogen Interactions; D006801:Humans; D057131:Immune Evasion; D007113:Immunity, Innate; D008264:Macrophages / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D008554:Melioidosis / Q000235:genetics / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000276:immunology; D010588:Phagosomes / Q000737:chemistry / Q000235:genetics / Q000276:immunology*; D015398:Signal Transduction; D025801:Ubiquitin / Q000235:genetics / Q000276:immunology
chemical_list: D001426:Bacterial Proteins; C477012:MAP1LC3A protein, human; D008869:Microtubule-Associated Proteins; D025801:Ubiquitin