Role of Interleukin-6 in Toll-Like Receptor 4 and 2 Expressions Induced by Lipopolysaccharide in the Lung |
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| Authors: | Ken-Ichiro Inoue Hirohisa Takano Rie Yanagisawa Miho Sakurai Akinori Shimada Takehito Morita |
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| Affiliation: | 1. Environmental Health Sciences Division, National Institute for Environmental Studies, Tsukuba, Japan;2. Inflammation and Immunology, Kyoto Prefectural University of Medicine, Kyoto, Japan;3. Department of Veterinary Pathology, Faculty of Agriculture, Tottori University, Tottori, Japan |
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| Abstract: | Our previous study demonstrated that interleukin (IL)-6 is protective against hemorrhagic lung inflammation induced by lipopolysaccharide (LPS) in mice, at least partly, by inhibition of the enhanced expressions of proinflammatory cytokines. The present study elucidated the role of IL-6 in Toll like receptor (TLR) 4 and 2 expressions in the lung during inflammation induced by intraperitoneal administration of LPS (1 mg/kg) using IL-6 null (-/-) mice and wild type (WT) mice. The expressions of mRNA for both TLR4 and 2 in the lung were evaluated 72 hrs after intraperitoneal administration. LPS enhanced both TLR4 mRNA expression as compared with vehicle. However, the enhancement was significantly stronger in IL-6 (-/-) mice than in WT mice after LPS challenge. LPS significantly increased TLR2 mRNA expression only in IL-6 (-/-) mice. As well, in the presence of LPS, the expression was significantly greater in IL-6 (-/-) mice than in WT mice. These results suggest that the protective role of IL-6 against LPS-induced hemorrhagic lung inflammation might be explained, in part, by inhibition of the enhanced lung expressions of TLR4 and 2. |
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| Keywords: | Interleukin-6 Lipopolysaccharide Lung Inflammation mRNA Toll-like receptor |
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