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Am J Physiol Heart Circ Physiol 279: H2241-H2248, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 5, H2241-H2248, November 2000

Expression and self-regulatory function of cardiac interleukin-6 during endotoxemia

Hiroshi Saito2, Cam Patterson1, Zhaoyong Hu1, Marschall S. Runge1, Ulka Tipnis3, Mala Sinha2, and John Papaconstantinou2

1 Sealy Center for Molecular Cardiology and 2 Department of Human Biological Chemistry and Genetics and 3 Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555

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.

heart; cytokines; inflammation; sepsis; interleukin 6-knockout mice


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