The effects of recombinant human beta-defensin-3 on expression of interleukin-17A and interleukin-22 in BEAS-2B cell.
- Author:
Bing-Ya GUO
1
;
Guang-Cheng XIE
1
;
Zhao-Jun DUAN
1
;
Li-Jun XIA
1
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line; Humans; Interleukin-17; genetics; metabolism; Interleukins; genetics; metabolism; RNA, Messenger; genetics; metabolism; Toll-Like Receptor 2; genetics; metabolism; beta-Defensins; genetics; metabolism
- From: Chinese Journal of Experimental and Clinical Virology 2013;27(4):260-262
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo research the effects of recombinant human beta-defensin-3 (hBD-3) on expression of interleukin-17A (IL-17A) and interleukin-22 (IL-22) in BEAS-2B cell.
METHODSThe BEAS-2B cells were stimulated with different concentrations of hBD-3 for 6 hours and 24 hours, respectively. Toll-like receptor 2 (TLR2), IL-17A and IL-22 mRNA expression levels were determined by real-time PCR, and the expression levels of IL-17A and IL-22 protein were examined by enzyme linked immune-sorbent assay.
RESULTSTLR2 mRNA in BEAS-2B cells were significantly increased in a concentration-and time-dependent manner after stimulating by hBD-3 for 24 hours compared to 6 hours. The IL-17A has significantly increased in mRNA and protein levels stimulated 24 hours in a concentration of 100 ng/ml, however, IL-17A mRNA expression has increased while protein didn't change stimulated 6 hours in a concentration of 50 ng/ml. The IL-22 mRNA and protein expression reached peak levels after stimulating in a concentration of 50 ng/ml of hBD-3 while IL-22 expression declined in mRNA and protein levels as the concentration of hBD-3 increased.
CONCLUSIONSRecombinant hBD-3 can up-regulated the expression of TLR2, IL-17A and IL-22, lower concentration of hBD-3 mainly increased the expression of IL-22 while higher concentration of hBD-3 mainly increased the expression of IL-17A. These results show that different concentrations of hBD-3 maybe activate different transcription factors which was mediated by TLR2, initiating host immune response.