T
Tomohiko Ogawa
Researcher at Asahi University
Publications - 118
Citations - 13431
Tomohiko Ogawa is an academic researcher from Asahi University. The author has contributed to research in topics: Porphyromonas gingivalis & Lipid A. The author has an hindex of 41, co-authored 118 publications receiving 13057 citations. Previous affiliations of Tomohiko Ogawa include Osaka University.
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Journal Article
Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product.
Katsuaki Hoshino,Osamu Takeuchi,Taro Kawai,Hideki Sanjo,Tomohiko Ogawa,Yoshifumi Takeda,Kiyoshi Takeda,Shizuo Akira +7 more
TL;DR: It is demonstrated that TLR4 is the gene product that regulates LPS response, and a single point mutation of the amino acid that is highly conserved among the IL-1/Toll receptor family is found.
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Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components.
Osamu Takeuchi,Katsuaki Hoshino,Taro Kawai,Hideki Sanjo,Haruhiko Takada,Tomohiko Ogawa,Kiyoshi Takeda,Shizuo Akira +7 more
TL;DR: It is demonstrated that TLR2 and TLR4 recognize different bacterial cell wall components in vivo andTLR2 plays a major role in Gram-positive bacterial recognition.
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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.
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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.
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Gene Expressions of Toll-Like Receptor 2, But Not Toll-Like Receptor 4, Is Induced by LPS and Inflammatory Cytokines in Mouse Macrophages
TL;DR: Results indicate that TLR2, in contrast to TLR4, can be induced in macrophages in response to bacterial infections and may accelerate the innate immunity against pathogens.