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Effects of CD38 gene on TLR4 and inflammatory cytokines and its mechanisms (835.10)
Author(s) -
Li Rong,
Chen Cheng,
Li Ling,
Li Li,
Kong Yuan,
Yang Xiao,
Liao Jie
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.835.10
Subject(s) - spleen , tlr4 , tumor necrosis factor alpha , cd38 , monocyte , inflammation , proinflammatory cytokine , interleukin , immune system , biology , tlr2 , immunology , cytokine , microbiology and biotechnology , stem cell , cd34
Protective mechanisms of the host will be initiated by the activation of Toll‐like receptor (TLR), including the chemotaxis and activation of immune cells. TLR4 defection always accompanied with inflammation. CD38 gene is associated with myocardial infarction. However, impact of CD38 gene on TLR4 is not well defined. Objective To study the influences of CD38 gene to the distribution of TLR4 and it's effects and mechanisms on expression of TLR4 and inflamatory cytokines. Methods Distribution of TLR4 in organs (such as heart, liver spleen, lung, kidney, cerebrum, thymus and lymph node) of C57/B6 mice and CD38‐/‐ C57/B6 mice were elucidated by polymerase chain reaction (PCR), Different expression of TLR4 in spleen of C57/B6 mice and CD38‐/‐ C57/B6 mice was analyzed by realtime PCR and westernblot (WB). Expression of inflammatory cytokines such as tumor necrosis factor‐α (TNF‐α), monocyte chemotactic protein 1 (MCP‐1), Interleukin‐1 (IL‐6) and Interleukin‐1β (IL‐1β) in spleen were analyzed by realtime PCR individually. Different expression of NF‐ĸB in spleen was analyzed by WB. Results TLR4 distribute broadly in all of the above organs in both C57/B6 mice and CD38‐/‐ C57/B6 mice. But comparing to C57/B6 mice, CD38‐/‐ C57/B6 mice showed an significantly decrease in the expression of TLR4 on both mRNA and protein level in spleen. Expression of inflammatory cytokines such as TNF‐α, MCP‐1 and IL‐6 were found to be significantly decreased accompanied by significantly increased expression of IL‐1β in spleen. Meanwhile, the expression of NF‐ĸB in spleen was greatly enhanced. Conclusions Overall, these data suggest that CD38 has a profound influence on TLR4, which may contribute to the dysregulated expression of inflammatory factors under physiological and such pathological conditions as myocardial infarction through NF‐ĸB pathway. Grant Funding Source : Supported by GJJ81302600 and 30960357