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- 저자 : Naohiro Inohara (검색결과 3 건)
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Zhao, Ling,Kwon, Myung-Ja,Huang, Shurong,Lee, Joo Y.,Fukase, Koichi,Inohara, Naohiro,Hwang, Daniel H. American Society for Biochemistry and Molecular Bi 2007 The Journal of biological chemistry Vol.282 No.16
<P>Nucleotide-binding oligomerization domain-containing proteins (Nods) are intracellular pattern recognition receptors recognizing conserved moieties of bacterial peptidoglycan through their leucine-rich repeats domain. The agonists for Nods activate proinflammatory signaling pathways, including NF-kappaB pathways. The results from our previous studies showed that the activation of TLR4 and TLR2, leucine-rich repeat-containing pattern recognition receptors, were differentially modulated by saturated and n-3 polyunsaturated fatty acids in macrophages and dendritic cells. Here, we show the differential modulation of NF-kappaB activation and interleukin-8 (IL-8) expression in colonic epithelial cells HCT116 by saturated and unsaturated fatty acids mediated through Nods proteins. Lauric acid (C12:0) dose dependently activated NF-kappaB and induced IL-8 expression in HCT116 cells, which express both Nod1 and Nod2, but not detectable amounts of TLR2 and TLR4. These effects of lauric acid were inhibited by dominant negative forms of Nod1 or Nod2, but not by dominant negative forms of TLR2, TLR4, and TLR5. The effects of lauric acid were also attenuated by small RNA interference targeting Nod1 or Nod2. In contrast, polyunsaturated fatty acids, especially n-3 polyunsaturated fatty acids, inhibited the activation of NF-kappaB and IL-8 expression induced by lauric acid or known Nods ligands in HCT116. Furthermore, lauric acid induced, but docosahexaenoic acid inhibited lauric acid- or Nod2 ligand MDP-induced, Nod2 oligomerization in HEK293T cells transfected with Nod2. Together, these results provide new insights into the role of dietary fatty acids in modulating inflammation in colon epithelial cells. The results suggest that Nods may be involved in inducing sterile inflammation, one of the key etiological conditions in the development of many chronic inflammatory diseases.</P>
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Shigeki Bamba,Osamu Inatomi,Atsushi Nishida,Masashi Ohno,Takayuki Imai,Kenichiro Takahashi,Yuji Naito,Junichi Iwamoto,Akira Honda,Naohiro Inohara,Akira Andoh 대한장연구학회 2022 Intestinal Research Vol.20 No.3
Background/Aims: Crosstalk between the gut microbiota and bile acid plays an important role in the pathogenesis of gastrointestinal disorders. We investigated the relationship between microbial structure and bile acid metabolism in the ileal mucosa of Crohn’s disease (CD).Methods: Twelve non-CD controls and 38 CD patients in clinical remission were enrolled. Samples were collected from the distal ileum under balloon-assisted enteroscopy. Bile acid composition was analyzed by liquid chromatography-mass spectrometry. The gut microbiota was analyzed by 16S rRNA gene sequencing.Results: The Shannon evenness index was significantly lower in endoscopically active lesions than in non-CD controls. β-Diversity, evaluated by the UniFrac metric, revealed a significant difference between the active lesions and non-CD controls (<i>P</i>=0.039). The relative abundance of <i>Escherichia</i> was significantly higher and that of <i>Faecalibacterium</i> and <i>Roseburia</i> was significantly lower in CD samples than in non-CD controls. The increased abundance of <i>Escherichia</i> was more prominent in active lesions than in inactive lesions. The proportion of conjugated bile acids was significantly higher in CD patients than in non-CD controls, but there was no difference in the proportion of primary or secondary bile acids. The genera <i>Escherichia</i> and <i>Lactobacillus</i> were positively correlated with the proportion of conjugated bile acids. On the other hand, <i>Roseburia</i>, <i>Intestinibacter</i>, and <i>Faecalibacterium</i> were negatively correlated with the proportion of conjugated bile acids.Conclusions: Mucosa-associated dysbiosis and the alteration of bile acid composition were identified in the ileum of CD patients. These may play a role in the pathophysiology of ileal lesions in CD patients.
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Kim, Donghyun,Seo, Sang-Uk,Zeng, Melody Y.,Kim, Wan-Uk,Kamada, Nobuhiko,Inohara, Naohiro,Nú,ú,ñ,ez, Gabriel The American Association of Immunologists, Inc. 2017 JOURNAL OF IMMUNOLOGY Vol.199 No.4
<P>Enteric pathogens including Salmonella enteric serovar Typhimurium can breach the epithelial barrier of the host and spread to systemic tissues. In response to infection, the host activates innate immune receptors via the signaling molecule MyD88, which induces protective inflammatory and antimicrobial responses. Most of these innate immune responses have been studied in hematopoietic cells, but the role of MyD88 signaling in other cell types remains poorly understood. Surprisingly, we found that Dermo1-Cre;Myd88(fl/fl) mice with mesenchymal cell-specific deficiency of MyD88 were less susceptible to orogastric and i.p. S. Typhimurium infection than their Myd88(fl/fl) littermates. The reduced susceptibility of Dermo1-Cre; Myd88(fl/fl) mice to infection was associated with lower loads of S. Typhimurium in the liver and spleen. Mutant analyses revealed that S. Typhimurium employs its virulence type III secretion system 2 to promote its growth through MyD88 signaling pathways in mesenchymal cells. Inflammatory monocytes function as a major cell population for systemic dissemination of S. Typhimurium. Mechanistically, mesenchymal cell-specific MyD88 signaling promoted CCL2 production in the liver and spleen and recruitment of inflammatory monocytes to systemic organs in response to S. Typhimurium infection. Consistently, MyD88 signaling in mesenchymal cells enhanced the number of phagocytes including Ly6C(hi)Ly6G(-) inflammatory monocytes harboring S. Typhimurium in the liver. These results suggest that S. Typhimurium promotes its systemic growth and dissemination through MyD88 signaling pathways in mesenchymal cells.</P>
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