Study of expression and regulation of TLR2/4 in mycobacterium tuberculosis heat shock proteins 16. 3 effect on mouse bone marrow-derived macrophages
10.3969/j.issn.1000-484X.2017.01.007
- VernacularTitle:TLR2/4在 MTB Hsp16.3刺激小鼠巨噬细胞过程中表达及作用的初步探讨
- Author:
Shanshan LI
;
Huan QIN
;
Qianyi LIU
;
Lin XU
;
Jidong ZHANG
;
Jihong FENG
;
Longmei LI
;
Hongfei PAN
;
Junmin LUO
- Keywords:
Mycobacterium tuberculosis;
Toll like receptors;
Mycobacterium tuberculosis heat shock proteins 16. 3;
Alternatively activated macrophage
- From:
Chinese Journal of Immunology
2017;33(1):36-40
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the expression and regulation of TLR2/4 in mycobacterium tuberculosis heat shock proteins 16. 3 (mycobacterium tuberculosis heat shock proteins 16. 3,MTB Hsp16. 3) effect on mouse bone marrow-derived macrophages in vitro. Methods:Bone marrow cells were isolated from tibia and femurs of BALB/c mice and incubated with GM-CSF,then detected the expression of CD11b and F4/80 with flow cytometry and observed morphology. The M0 macrophages were stimulated with MTB Hsp16. 3 for 0 h,12 h,24 h,36 h,48 h and 72 h. Real-time PCR detected the expression of TLR2/4 in intracellular at different time point. Silencing macrophages cell surface TLR2/4 molecules by siRNA technology which stimulated with MTB Hsp16. 3 for 0 h,12 h,24 h,36 h,48 h and 72 h. Real-time PCR detected the expression of TLR2/4,Ym-1,Fizz1,IL-10,TNF-α,iNOS and TGF-βin intracellular at different time point. Results:Morphology analysis showed that MTB Hsp16. 3 stimulated macrophages were round cells stretching out pseudopodia,whereas MTB Hsp16. 3 stimulated silencing TLR2/4 macrophages had elongated fibroblastoid. Real time PCR detected the expression of TLR2/4 were upregulated after MTB Hsp16. 3 stimulated M0 macrophages. MTB Hsp16. 3 stimulated silencing TLR2/4 macrophages the expression of IL-6, TNF-α, iNOS were upregulated, whereas IL-10, TGF-β, Ym-1 and Fizz1 were downregulated. Conclusion:MTB Hsp16. 3 may stimulated M0 macrophages to M2 macrophages and suppress M1 macrophages through binding with TLR2/4 receptor,which may be involved the progresss of MTB evaded macrophage phagocytosis.
