TY  - JOUR
N1  - Copyright of this article belongs to  American Association of Immunologists
ID  - open1855
UR  - http://www.jimmunol.org/content/197/1/244.long
IS  - 1
A1  - Bhagyaraj, Ella
A1  - Nanduri, Ravikanth
A1  - Saini, Ankita
A1  - Dkhar, Hedwin Kitdorlang
A1  - Ahuja, Nancy
A1  - Chandra, Vemika
A1  - Mahajan, Sahil
A1  - Kalra, Rashi
A1  - Tiwari, Drishti
A1  - Sharma, Charu
A1  - Janmeja, Ashok Kumar
A1  - Gupta, Pawan
Y1  - 2016/07/01/
N2  - 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.
PB  -  American Association of Immunologists
JF  - Journal of immunology 
VL  - 197
SN  - 1550-6606
TI  - Human Xenobiotic Nuclear Receptor PXR Augments Mycobacterium tuberculosis Survival.
SP  - 244
EP  - 55
ER  -