Lipolytic enzymes in Mycobacterium tuberculosis

Abstract

Mycobacterium tuberculosis is a bacterial pathogen that can persist for decades in an infected patient without causing a disease. In vivo, the tubercle bacillus present in the lungs store triacylglycerols in inclusion bodies. The same process can be observed in vitro when the bacteria infect adipose tissues. Indeed, before entering in the dormant state, bacteria accumulate lipids originating from the host cell membrane degradation and from de novo synthesis. During the reactivation phase, these lipids are hydrolysed and the infection process occurs. The degradation of both extra and intracellular lipids can be directly related to the presence of lipolytic enzymes in mycobacteria, which have been ignored during a long period particularly due to the difficulties to obtain a high expression level of these enzymes in M. tuberculosis. The completion of the M. tuberculosis genome offered new opportunity to this kind of study. The aim of this review is to focus on the recent results obtained in the field of mycobacterium lipolytic enzymes and although no experimental proof has been shown in vivo, it is tempting to speculate that these enzymes could be involved in the virulence and pathogenicity processes.

Mycobacterial Pathogenomics and Evolution

“…The presence of enzymes that are predicted to show lipolytic functions further suggests that M. tuberculosis might use host-cell lipids and sterols as energy sources via the β-oxidation cycle, a pathway that is required for lipid catabolism. The M. tuberculosis genome contains genes for more than 100 enzymes that might be involved in various lipid oxidation pathways used for metabolizing putative degradation products of host cell membranes (10,20,21).…”

A study of correlation between tuberculosis and gall bladder pathology

“…In-vivo, it persists within macrophages by storing triacylglycerols in inclusion bodies. 24 Similar process occurs in-vitro when these bacilli infect adipose tissue. In dormant state, Mycobacterium tuberculosis accumulates lipids for their survival which are hydrolysed during reactivation phase.…”

Rv3802c in Tuberculosis Therapeutics

“…The current scenario of tuberculosis might be dealt by targeting pathogen's enzymes that participate in both cell wall and lipid metabolism [6][7][8].…”

“…The current scenario of tuberculosis might be dealt by targeting pathogen's enzymes that participate in both cell wall and lipid metabolism [6][7][8].Rv3802c is such a drug target which gained importance due to its genetic location in a mycolic acid synthesis proved essentiality from mutagenesis experiments [9]. Conditional disruptions of MSMEG_6394, functional homolog of Rv3802c in M. smegmatis lead to loss of cell wall integrity and internal structure of cell.…”