AI Article Synopsis
- - This study explores how *Mycobacterium tuberculosis* (M. tuberculosis) can evade the immune system, focusing on the role of the human nuclear receptor pregnane X receptor (PXR) in its survival in macrophages.
- - Researchers found that PXR enhances M. tuberculosis survival by promoting foamy macrophage formation and preventing important immune processes like phagolysosomal fusion, inflammation, and apoptosis.
- - Using a mouse model that expresses human PXR, the study suggests that targeting hPXR with pharmacological treatments could be a potential new strategy for tuberculosis therapy.
Article Abstract
Mycobacterium tuberculosis can evade host defense processes, thereby ensuring its survival and pathogenesis. In this study, we investigated the role of nuclear receptor, pregnane X receptor (PXR), in M. tuberculosis infection in human monocyte-derived macrophages. In this study, we demonstrate that PXR augments M. tuberculosis survival inside the host macrophages by promoting the foamy macrophage formation and abrogating phagolysosomal fusion, inflammation, and apoptosis. Additionally, M. tuberculosis cell wall lipids, particularly mycolic acids, crosstalk with human PXR (hPXR) by interacting with its promiscuous ligand binding domain. To confirm our in vitro findings and to avoid the reported species barrier in PXR function, we adopted an in vivo mouse model expressing hPXR, wherein expression of hPXR in mice promotes M. tuberculosis survival. Therefore, pharmacological intervention and designing antagonists to hPXR may prove to be a promising adjunct therapy for tuberculosis.
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| http://dx.doi.org/10.4049/jimmunol.1600203 | DOI Listing |
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