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Review
. 2018 Jul 26:23:63.
doi: 10.4103/jrms.JRMS_904_17. eCollection 2018.

Mycobacterium tuberculosis and lipids: Insights into molecular mechanisms from persistence to virulence

Affiliations
Review

Mycobacterium tuberculosis and lipids: Insights into molecular mechanisms from persistence to virulence

Ciamak Ghazaei. J Res Med Sci. .

Abstract

Mycobacterium tuberculosis is a causative agent of tuberculosis that causes deaths across the world. The pathogen apart from causing disease manifestations can also enter into a phase of latency to re-emerge later. Among the various factors associated with the virulence of pathogen, the lipids composing the cell wall of the bacillus have drawn much interest among. The unique composition of the cell wall composed of mycolic acid, glycolipids such as diacyltrehaloses, polyacyltrehalose, lipomannan, lipoarabinomannan (LAM), mannose-capped-LAM, sulfolipids, and trehalose-6,6'-dimycolate, all have been implicated in providing the pathogen an advantage in the host. The pathogen also alters its metabolism of fatty acids to survive the conditions in the host that is reflected in an altered cell wall composition in terms of lipids. In addition, the lipid profile of the cell wall has been shown to modulate the immune responses launched by the host, especially in the suppression, or production of inflammatory factors, cytokines, and phagocytic cells, such as dendritic cells and macrophages. Apart from M. tuberculosis, the paper also briefly looks at the role of Mycobacterium bovis and its role in tuberculosis in humans along with its lipid profile of its cell wall. This review aims to summarize the various lipids of the cell wall of M. tuberculosis along with their roles in enabling the pathogen to maintain its virulence to infect further humans and its persistence inside the host.

Keywords: Cell wall lipids of Mycobacterium bovis; Mycobacterium tuberculosis; glycolipids and pathogenicity; lipids of cell wall; persistence; role of lipids in virulence.

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Conflict of interest statement

There are no conflicts of interest.

Figures

Figure 1
Figure 1
The lipid-rich cell wall of Mycobacterium tuberculosis
Figure 2
Figure 2
The timeline model of bacterial lipid-regulated host immunological response to infection

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