OBJECTIVE: To investigate the synthesis of IL 13 in cultured human mesangial cells (HMC) following LPS activation and the inhibitory effect of IL 13 on the pro inflammatory cytokines, chemokines, and pro fibrogentic cytokine expression by HMC. METHODS: The expression of IL 13 mRNA and production of IL 13 protein were determined using the semiquantitative reverse transcription PCR technique and ELISA respectively. TNF α, IL 1α, IL 1β, MCP 1, IL 8, and TGF β1 mRNA expressions were determined by ribonuclease protection assay. RESULTS: ①Basal levels of IL 13 were undetectable and HMC stimulated with LPS produced IL 13 in a dose dependent manner. ②HMC which was incubated in the medium alone did not express IL 1α and MCP 1 mRNA, and constitutive mRNA expression in unstimulated cells was found for TNF α, IL 1β, IL 8, and TGF β1. LPS significantly upregulated TNF α, IL 1α, IL 1β, MCP 1, IL 8, and TGF β1 mRNA expressions. Recombinant human IL 13 inhibited TNF α, IL 1α, IL 1β, MCP 1, IL 8, and TGF β1 mRNA expressions in a dose dependent manner. CONCLUSIONS: LPS can synergistically induce the expression of IL 13 in HMC. IL 13 can inhibit pro inflammatory cytokines, chemokines and profibrogenic cytokine synthesis, which suggests that IL 13 has important regulatory effects on the inflammatory response of HMC."/>
系膜细胞来源的IL-13对系膜细胞促炎性细胞因子基因表达的调控作用
Abstract：OBJECTIVE: To investigate the synthesis of IL 13 in cultured human mesangial cells (HMC) following LPS activation and the inhibitory effect of IL 13 on the pro inflammatory cytokines, chemokines, and pro fibrogentic cytokine expression by HMC. METHODS: The expression of IL 13 mRNA and production of IL 13 protein were determined using the semiquantitative reverse transcription PCR technique and ELISA respectively. TNF α, IL 1α, IL 1β, MCP 1, IL 8, and TGF β1 mRNA expressions were determined by ribonuclease protection assay. RESULTS: ①Basal levels of IL 13 were undetectable and HMC stimulated with LPS produced IL 13 in a dose dependent manner. ②HMC which was incubated in the medium alone did not express IL 1α and MCP 1 mRNA, and constitutive mRNA expression in unstimulated cells was found for TNF α, IL 1β, IL 8, and TGF β1. LPS significantly upregulated TNF α, IL 1α, IL 1β, MCP 1, IL 8, and TGF β1 mRNA expressions. Recombinant human IL 13 inhibited TNF α, IL 1α, IL 1β, MCP 1, IL 8, and TGF β1 mRNA expressions in a dose dependent manner. CONCLUSIONS: LPS can synergistically induce the expression of IL 13 in HMC. IL 13 can inhibit pro inflammatory cytokines, chemokines and profibrogenic cytokine synthesis, which suggests that IL 13 has important regulatory effects on the inflammatory response of HMC.
