The immune response of human keratinocytes to Trichophyton rubrum conidia is partially mediated by toll-like receptor-2, 4, dectin-1 and cytokines.
- Author:
Ying LI
1
;
Jian CHEN
;
Miao-Jian WAN
;
Wei LAI
;
Yue ZHENG
;
Mei-Rong LI
;
Rong-Zhang CHEN
;
Xiao-Xin LI
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line; Chemokine CCL1; secretion; Coculture Techniques; Humans; Interferon-gamma; secretion; Interleukin-13; secretion; Interleukin-6; secretion; Interleukin-8; secretion; Keratinocytes; metabolism; Lectins, C-Type; metabolism; Toll-Like Receptor 2; metabolism; Toll-Like Receptor 4; metabolism; Trichophyton; Tumor Necrosis Factor-alpha; secretion
- From: Journal of Southern Medical University 2011;31(4):678-681
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of Trichophyton rubrum exposure on the expressions of toll-like receptor-2 (TLR-2), TLR-4 and dendritic cell associated C-type lectin-1 (Dectin-1) and cytokine secretions in human keratinocytes cell line HaCaT.
METHODSThe mRNA of TLR-2,4, and dectin-1 in the HaCaT co-cultured with the conidia of Trichophyton rubrum conidia for 24 h was measured with real-time PCR. The mean fluorescence intensity and the percentage of cells positive for TLR-2, 4, and dectin-1 was detected during the co-culture using flow cytometry. The cytokine secretion profiles in the cell culture supernatant was analyzed using a cytokine antibody array.
RESULTSThe TLR-2,4, and dectin-1 mRNA expressions, mean fluorescence intensity and percentage of positive cells for TLR-2,4, and dectin-1 all increased in HaCaT cells in response to Trichophyton rubrum conidia exposure. The results of cytokine antibody array demonstrated obviously increased secretions of IL-8, I-309, IFN-γ, IL-6, and IL-13 in the culture supernatant of HaCaT cells in response to Trichophyton rubrum exposure.
CONCLUSIONThe immune responses and immunological recognition of human keratinocytes to Trichophyton rubrum conidia are partially mediated by up-regulating the expressions of TLR-2, TLR-4 and dectin-1 and secretions of multiple cytokines.
