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Abstract
Autophagy is a self-degradative process that removes misfolded or aggregated proteins, clears damaged organelles, as well as eliminates intracellular pathogens playing a role in innate immunity. Mycobacterium abscessus (M. abscessus) has been reported as a causative organism in nearly 80% of the rapid growing mycobacteria (RGM) pulmonary disease. The strain exhibits two different colony types: the smooth (S) one which is considered wild-type and the rough (R) one which is the mutated strain. In accordance to the colony morphology, the S and R types display varying autophagic responses in the host cells with the R type inducing elevated autophagy compared to the S type. The major difference in the autophagy could be based on the bioactive molecules exposed on the surface of the S and R types. Though autophagy has a vital role to play in the clearance of intracellular pathogens, very little is known on the autophagy induced by M. abscessus. It has been known that the intracellular pathogens employ different strategies to evade the autophagic pathway and to survive within the host cells. This review summarizes the most up-to-date findings on autophagy induced by M. abscessus morphotypes and how M. abscessus evades the autophagic machinery to divide and thrive inside the host cells. In addition, the prospects of autophagic machinery in devising new anti-infective strategies against mycobacterial infection is also been discussed.
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Figure 1.
Proposed model of the autophagic pathway in response to S and R type M. abscessus infiltration. After invasion, the bacteria are contained in endosomes. The R type endosomes are characterized by the presence of multiple bacterial cells in contrast to the S type. The endosomes fuse with early autophagosomes which later matures into late autophagosomes. The late autophagosomes eventually fuse with the lysosomes to become autolysosomes in which the bacteria are killed. The R type M. abscessus inhibits lysosomal fusion and replicate within replicating vacuoles that resemble late autophagosomes.
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