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The unique PE/PPE multigene family of proteins occupies almost 10% of the coding sequence of  Mycobacterium tuberculosis  ( M.tb ), the causative agent of human tuberculosis. Although some members of this family have been shown to be involved in pathways essential to  M.tb  pathogenesis, their precise physiological functions remain largely undefined. Here, we investigate the roles of the conserved members of the ‘PE only’ subfamily Rv0285 (PE5) and Rv1386 (PE15) in mediating host-pathogen interactions. Recombinant  Mycobacterium smegmatis  strains expressing PE5 and PE15 showed enhanced survival  vs  controls in J774.1 and THP-1 macrophages - this increase in viable counts was correlated with a reduction in transcript levels of inducible nitric oxide synthase. An up-regulation of anti- and down-regulation of pro-inflammatory cytokine levels was also observed in infected macrophages implying an immuno-modulatory function for these proteins. Induction of IL-10 production upon infection of THP-1 macrophages was associated with increased phosphorylation of the MAP Kinases p38 and ERK1/2, which was abolished in the presence of the pharmacological inhibitors SB203580 and PD98059. The  PE5-PPE4  and  PE15-PPE20  gene pairs were observed to be co-operonic in  M.tb , hinting at an additional level of complexity in the functioning of these proteins. We conclude that  M.tb  exploits the PE proteins to evade the host immune response by altering the Th1 and Th2 type balance thereby favouring  in vivo  bacillary survival.

The Mycobacterium tuberculosis PE Proteins Rv0285 and Rv1386 Modulate Innate Immunity and Mediate Bacillary Survival in Macrophages