BACKGROUND/AIMS: The increased expression of several cytokines, including interleukin 6 (IL-6), has recently been reported in a study of the longitudinal muscle and myenteric plexus layers of rat intestine following Trichinella spiralis infection. However, the putative cellular sources and the mechanism underlying the induction of IL-6 in these tissues are presently unknown. The aim of this study was to examine the ability of cultured smooth muscle cells from rat jejunum to produce IL-6 messenger RNA and protein and to investigate the underlying mechanism. METHODS: Cultured smooth muscle cells were treated with human recombinant interleukin 1 beta (HrIL-1 beta). The level of IL-6 messenger RNA was estimated by polymerase chain reaction, and the released IL-6 protein was estimated by bioassay. RESULTS: HrIL-1 beta induced IL-6 messenger RNA expression in the smooth muscle cells in a time- and concentration-dependent manner. This was accompanied by the secretion of IL-6 protein into the medium. The effect of HrIL-1 beta was blocked by the IL-1 receptor antagonist, by actinomycin D, or by prior boiling of the cytokine. CONCLUSIONS: These findings show that HrIL-1 beta interacts with its receptor on smooth muscle cells to induce transcription of the IL-6 gene and to cause the secretion of IL-6. These results indicate that intestinal smooth muscle cells are not only targets for but also a source of cytokine.
BACKGROUND/AIMS: The increased expression of several cytokines, including interleukin 6 (IL-6), has recently been reported in a study of the longitudinal muscle and myenteric plexus layers of rat intestine following Trichinella spiralis infection. However, the putative cellular sources and the mechanism underlying the induction of IL-6 in these tissues are presently unknown. The aim of this study was to examine the ability of cultured smooth muscle cells from rat jejunum to produce IL-6 messenger RNA and protein and to investigate the underlying mechanism. METHODS: Cultured smooth muscle cells were treated with human recombinant interleukin 1 beta (HrIL-1 beta). The level of IL-6 messenger RNA was estimated by polymerase chain reaction, and the released IL-6 protein was estimated by bioassay. RESULTS: HrIL-1 beta induced IL-6 messenger RNA expression in the smooth muscle cells in a time- and concentration-dependent manner. This was accompanied by the secretion of IL-6 protein into the medium. The effect of HrIL-1 beta was blocked by the IL-1 receptor antagonist, by actinomycin D, or by prior boiling of the cytokine. CONCLUSIONS: These findings show that HrIL-1 beta interacts with its receptor on smooth muscle cells to induce transcription of the IL-6 gene and to cause the secretion of IL-6. These results indicate that intestinal smooth muscle cells are not only targets for but also a source of cytokine.
Authors: Edmond K Ng; Ninder Panesar; Walter E Longo; Marc J Shapiro; Donald L Kaminski; Kym C Tolman; John E Mazuski Journal: Mediators Inflamm Date: 2003-02 Impact factor: 4.711
Authors: Jeffrey S Otis; Sarah Niccoli; Nicole Hawdon; Jessica L Sarvas; Melinda A Frye; Adam J Chicco; Simon J Lees Journal: PLoS One Date: 2014-03-19 Impact factor: 3.240