Preliminary study of the expression and regulation of TLR2/4 in mycobacterium tuberculosis heat shock proteins 16.3 effect on mouse bone marrow–derived macrophages
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- 英文论文题名：Preliminary study of the expression and regulation of TLR2/4 in mycobacterium tuberculosis heat shock proteins 16.3 effect on mouse bone marrow–derived macrophages
- 论文作者：LI Shan-Shan ; QIN Huan ; LIU Qian-Yi ; XU Lin ; ZHANG Ji-Dong ; FENG Ji-Hong ; LI Long-Mei ; PANG Hong-Fei ; LUO Jun-Min
- 英文论文作者：LI Shan-Shan ; QIN Huan ; LIU Qian-Yi ; XU Lin ; ZHANG Ji-Dong ; FENG Ji-Hong ; LI Long-Mei ; PANG Hong-Fei ; LUO Jun-Min ; Department of Immunology ; Zunyi Medical College ; Immune molecules application research center in Guizhou Province
- 年：2016
- 作者机构：Department of Immunology,Zunyi Medical College,Immune molecules application research center in Guizhou Province;
- 英文论文关键词：Mycobacterium tuberculosis ; Toll like receptors ; Mycobacterium tuberculosis heat shock proteins 16.3
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R378.911
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：378k
- 原文格式：D
- 会议级别：全国
摘要
Objective: Preliminary study of 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 detects the expression of CD11 b and F4/80 with flow cytometry and observes morphology;The M0 macrophages were stimulated with MTB Hsp16.3 for 0h,12 h,24h,36 h,48h 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 0h,12 h,24h,36 h,48h and 72 h. Real time PCR detected the expression of TLR2/4,Ym-1,Fizz1,IL-10,TNF-α, i NOS 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-a,i NOS were upregulated, whereas IL-10,TGF-β,Ym-1 and Fizz1 were downregulated. Conclusion:Together,these data indicated that 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.
Objective: Preliminary study of 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 detects the expression of CD11 b and F4/80 with flow cytometry and observes morphology;The M0 macrophages were stimulated with MTB Hsp16.3 for 0h,12 h,24h,36 h,48h 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 0h,12 h,24h,36 h,48h and 72 h. Real time PCR detected the expression of TLR2/4,Ym-1,Fizz1,IL-10,TNF-α, i NOS 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-a,i NOS were upregulated, whereas IL-10,TGF-β,Ym-1 and Fizz1 were downregulated. Conclusion:Together,these data indicated that 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.
Objective: Preliminary study of 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 detects the expression of CD11 b and F4/80 with flow cytometry and observes morphology;The M0 macrophages were stimulated with MTB Hsp16.3 for 0h,12 h,24h,36 h,48h 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 0h,12 h,24h,36 h,48h and 72 h. Real time PCR detected the expression of TLR2/4,Ym-1,Fizz1,IL-10,TNF-α, i NOS 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-a,i NOS were upregulated, whereas IL-10,TGF-β,Ym-1 and Fizz1 were downregulated. Conclusion:Together,these data indicated that 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.
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