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Expression of toll‐like receptors in T lymphocytes stimulated with N ‐(3‐oxododecanoyl)‐L‐homoserine lactone from Pseudomonas aeruginosa
Author(s) -
Bao Lei,
Yu Jialin,
Zhong Haiying,
Huang Daochao,
Lu Qi
Publication year - 2017
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12690
Subject(s) - pseudomonas aeruginosa , immune system , microbiology and biotechnology , biology , receptor , peripheral blood mononuclear cell , toll like receptor , tumor necrosis factor alpha , inflammation , lymphocyte , immunology , innate immune system , bacteria , in vitro , biochemistry , genetics
The establishment of chronic Pseudomonas aeruginosa infections is correlated with the disturbance of the host immune system. The P. aeruginosa quorum‐sensing molecule N ‐3‐(oxododecanoyl)‐L‐homoserine lactone (3‐O‐C12‐ HSL ) has the potential to modulate the host immune system. The immune system recognizes pathogens via toll‐like receptors ( TLR s). We found that 3‐O‐C12‐ HSL induced TLR changes in monocytes. However, the role of T cells in P. aeruginosa infection has not been delineated. In order to understand this activity, we examined whether 3‐O‐C12‐ HSL has an effect on the immune function and the expression of TLR s in T lymphocytes. Human peripheral blood mononuclear cells (PBMCs) cells were cultured with 0, 1, 10, 50, or 100 μM 3‐O‐C12‐HSL for 12 h. TLR 2/ TLR 4 expression and T‐lymphocyte proliferation were increased in a dose‐dependent manner, and 100 μM 3‐O‐C12‐ HSL significantly increased TLR 2 expression. Moreover, tumor necrosis factor‐α production of these PBMC s was inhibited. To conclude, 3‐O‐C12‐ HSL can induce lymphocyte cell proliferation. These findings provide a new perspective on our understanding of the persistence of the chronic inflammation that accompanies P. aeruginosa infection.