O
Osamu Adachi
Researcher at Hyogo College of Medicine
Publications - 18
Citations - 6391
Osamu Adachi is an academic researcher from Hyogo College of Medicine. The author has contributed to research in topics: Tympanoplasty & Receptor. The author has an hindex of 8, co-authored 17 publications receiving 6206 citations.
Papers
More filters
Journal ArticleDOI
Unresponsiveness of MyD88-Deficient Mice to Endotoxin
TL;DR: It is demonstrated that MyD88 knockout mice lack the ability to respond to LPS as measured by shock response, B cell proliferative response, and secretion of cytokines by macrophages and embryonic fibroblasts, and the inability of MyD 88 knockout mice to induce LPS-dependent gene expression cannot be attributed to lack of the activation of MAP kinases and NF-kappaB.
Journal ArticleDOI
Targeted Disruption of the MyD88 Gene Results in Loss of IL-1- and IL-18-Mediated Function
Osamu Adachi,Taro Kawai,Kiyoshi Takeda,Makoto Matsumoto,Hiroko Tsutsui,Masafumi Sakagami,Kenji Nakanishi,Shizuo Akira +7 more
TL;DR: It is demonstrated that MyD88 is a critical component in the signaling cascade that is mediated by IL-1 receptor as well as IL-18 receptor, and increases in interferon-gamma production and natural killer cell activity in response to IL- 18 are abrogated.
Journal ArticleDOI
Defective NK Cell Activity and Th1 Response in IL-18–Deficient Mice
Kiyoshi Takeda,Hiroko Tsutsui,Tomohiro Yoshimoto,Osamu Adachi,Nobuaki Yoshida,Tadamitsu Kishimoto,Haruki Okamura,Kenji Nakanishi,Shizuo Akira +8 more
TL;DR: The in vivo role of IL-18 and IL-12 in NK activity, as well as in in vivo Th1 response is demonstrated, demonstrating the important role of both IL- 18 andIL-12 as cytokine secreted from activated macrophages and induces IFNgamma production.
Journal ArticleDOI
Limb and Skin Abnormalities in Mice Lacking IKKα
Kiyoshi Takeda,Osamu Takeuchi,Tohru Tsujimura,Satoshi Itami,Osamu Adachi,Taro Kawai,Hideki Sanjo,Kunihiko Yoshikawa,Nobuyuki Terada,Shizuo Akira +9 more
TL;DR: There was no impairment of NF-kappaB activation induced by either interleukin-1 or tumor necrosis factor-alpha in IKKalpha-deficient embryonic fibroblasts and thymocytes, indicating that IKK alpha is not essential for cytokine-induced activation of NF.
Journal ArticleDOI
Cellular responses to bacterial cell wall components are mediated through MyD88-dependent signaling cascades.
TL;DR: Results show that MyD88 is essential for the cellular response to bacterial cell wall components and that macrophages and splenocytes from TLR4-deficient mice did not respond to any of the bacterial components the authors tested.