Despite increased pro-inflammation compared to the uninfected controls; there was no up-regulation of IFN-γ or the T cell chemoattractant CCL5 in the lung of patients with pulmonary TB.
The association of genetic variants of chemokines, CCL2 [MCP-1 (monocyte chemoattractant protein-1)], CCL5 [RANTES (regulated on activation, normal T-cell expressed and secreted)] and their receptors CCR2 and CCR5, respectively, earlier reported to be associated with susceptibility to pulmonary tuberculosis (PTB) in certain ethnic populations, were explored in Sahariya tribe, a primitive tribe of North Central India having a high prevalence of TB.
Peripheral blood mononuclear cells obtained from 21 pulmonary tuberculosis (PTB) patients and 24 healthy controls (HCs) were cultured for 48 h with culture filtrate antigen (CFA) of Mycobacterium tuberculosis with or without vitamin D(3) at a concentration 1 × 10(-7)M. The relative mRNA expression of monocyte chemoattractant protein-1 (MCP-1, CCL2), macrophage inflammatory protein-1α (MIP-1α, CCL3), macrophage inflammatory protein-1β (MIP-1β, CCL4), and regulated upon-activation, normal T cell-expressed and secreted (RANTES, CCL5) and IFN-γ inducible protein-10 (IP-10, CXCL10) chemokines were estimated from 48 h old macrophages using real-time polymerase chain reaction (RT-PCR).
Though the present results suggest that the CCL5 gene haplotype A-C-C and the diplotype G/A-T/C may be associated with resistance to PTB, further studies with increased sample size may be useful to confirm this present finding as well as to understand the role of CCL5 haplotype and diplotype on genetic susceptibility to TB.