Abstract
The lipid-rich cell wall of Mycobacterium tuberculosis is a dynamic structure that is involved in the regulation of the transport of nutrients, toxic host-cell effector molecules, and anti-tuberculosis drugs. It is therefore postulated to contribute to the long-term bacterial survival in an infected human host. Accumulating evidence suggests that M. tuberculosis remodels the lipid composition of the cell wall as an adaptive mechanism against host-imposed stress. Some of these lipid species (trehalose dimycolate, diacylated sulphoglycolipid, and mannan-based lipoglycans) trigger an immunopathologic response, whereas others (phthiocerol dimycocerosate, mycolic acids, sulpholipid-1, and di-and polyacyltrehalose) appear to dampen the immune responses. These lipids appear to be coordinately expressed in the cell wall of M. tuberculosis during different phases of infection, ultimately determining the clinical fate of the infection. This review summarizes the current state of knowledge on the metabolism, transport, and homeostatic or immunostatic regulation of the cell wall lipids, and their orchestrated interaction with host immune responses that results in bacterial clearance, persistence, or tuberculosis.
Highlights
Tuberculosis remains an important underlying cause of death from lung disease worldwide
The rate of relapse varies between 8-13%, depending on the prevalence of multidrugresistant tuberculosis (MDRTB) in that population[2]
It was thought that M. tuberculosis is engulfed by alveolar macrophages after entering the lungs, but the cellular architecture of the alveolar space suggests that M. tuberculosis will most likely interact with these pneumocytes first[3]
Summary
Bacterial immunostat: Mycobacterium tuberculosis lipids and their role in the host immune response. Laboratório Avançado de Saúde Pública, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, Bahia, Brasil
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