Different strains of Mycobacterium tuberculosis (M. tuberculosis) are known to modify the host immune response in a strain-specific manner. However, studies linking M. tuberculosis strain-specific impact upon the regulation of mitogen activated protein kinase (MAPK)-induced monocyte activation are limited. We have studied the immunomodulation, induced by a prevalent Indo-Oceanic Clade clinical strain S7, isolated from the Mycobacterium bovis bacillus Calmette–Guerin (BCG) trial area of Thiruvallur district, South India, in comparison with a low prevalent Beijing strain. It was shown that p38, stress-activated protein kinase/c-jun N-terminal kinases (SAPK/JNK) and extracellular signal-regulated kinases 1 and 2 (ERK1/2) of the MAPK pathways were not activated via cluster of differentiation 14 (CD14) and Human Leukocyte Antigen-DR (HLA-DR) receptors, upon infection of human monocytic cell line (THP-1) with clinical strain S7. The levels of proinflammatory cytokines, surface expression of CD44 and CD25 receptors, and the production of anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), varied between the strains. Inhibition experiments showed that the clinical strains use different signaling pathways to induce interleukin-6 (IL-6) secretion and surface expression of CD44. In addition, contrasting patterns were observed between strain-induced tumour necrosis alpha (TNF-α) and Bcl-2 levels. These data provided a precedent for effects of M. tuberculosis strain-specific factors upon the mechanisms involved in MAPK-mediated immune activation.
Key words: Mycobacterium tuberculosis, clinical isolate S7, Beijing strain, mitogen-activated protein kinases.
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