title: Role of interleukin-6 in toll-like receptor 4 and 2 expressions induced by lipopolysaccharide in the lung.
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.
authors.affiliation: Environmental Health Sciences Division, National Institute for Environmental Studies, Tsukuba, Japan.
authors.forename: Ken-Ichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Miho
authors.initials: M
authors.lastname: Sakurai
authors.forename: Akinori
authors.initials: A
authors.lastname: Shimada
authors.forename: Takehito
authors.initials: T
authors.lastname: Morita
authors.forename: Masahiko
authors.initials: M
authors.lastname: Sato
authors.forename: Shin
authors.initials: S
authors.lastname: Yoshino
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Yoshikawa
mesh_terms: D000818:Animals; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D006470:Hemorrhage / Q000139:chemically induced / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D007113:Immunity, Innate / Q000235:genetics; D015850:Interleukin-6 / Q000172:deficiency / Q000276:immunology / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000633:toxicity*; D051379:Mice; D018345:Mice, Knockout; D011014:Pneumonia / Q000139:chemically induced / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D051195:Toll-Like Receptor 2 / Q000096:biosynthesis* / Q000276:immunology; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis* / Q000276:immunology
chemical_list: D015850:Interleukin-6; D008070:Lipopolysaccharides; D012333:RNA, Messenger; C493486:Tlr2 protein, mouse; C493487:Tlr4 protein, mouse; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4