| First Author | Saito H | Year | 2000 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 279 |
| Issue | 5 | Pages | H2241-8 |
| PubMed ID | 11045959 | Mgi Jnum | J:108274 |
| Mgi Id | MGI:3623637 | Doi | 10.1152/ajpheart.2000.279.5.H2241 |
| Citation | Saito H, et al. (2000) Expression and self-regulatory function of cardiac interleukin-6 during endotoxemia. Am J Physiol Heart Circ Physiol 279(5):H2241-8 |
| abstractText | Interleukin (IL)-6 reportedly has negative inotropic and hypertrophic effects on the heart. Here, we describe endotoxin-induced IL-6 in the heart that has not previously been well characterized. An intraperitoneal injection of a bacterial lipopolysaccharide into C57BL/6 mice induced IL-6 mRNA in the heart more strongly than in any other tissue examined. Induction of mRNA for two proinflammatory cytokines, IL-1beta and tumor necrosis factor (TNF)-alpha, occurred rapidly before the induction of IL-6 mRNA and protein. Although stimulation of isolated rat neonatal myocardial cells with IL-1beta or TNF-alpha induced IL-6 mRNA in vitro, nonmyocardial heart cells produced higher levels of IL-6 mRNA upon stimulation with IL-1beta. In situ hybridization and immunohistochemical analyses localized the IL-6 expression primarily in nonmyocardial cells in vivo. Endotoxin-induced expression of cardiac IL-1beta, TNF-alpha, and intercellular adhesion molecule 1 was augmented in IL-6-deficient mice compared with control mice. Thus cardiac IL-6, expressed mainly by nonmyocardial cells via IL-1beta action during endotoxemia, is likely to suppress expression of proinflammatory mediators and to regulate itself via a negative feedback mechanism. |
