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Nucleotide-binding oligomerization domain 1 acts in concert with the cholecystokinin receptor agonist, cerulein, to induce IL-33-dependent chronic pancreatitis.
Watanabe, T; Sadakane, Y; Yagama, N; Sakurai, T; Ezoe, H; Kudo, M; Chiba, T; Strober, W.
Afiliación
  • Watanabe T; Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
  • Sadakane Y; Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
  • Yagama N; Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
  • Sakurai T; Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
  • Ezoe H; Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
  • Kudo M; Department of Gastroenterology and Hepatology, Kinki University Graduate School of Medicine, Osaka-sayama, Osaka, Japan.
  • Chiba T; Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
  • Strober W; Department of Gastroenterology and Hepatology, Kinki University Graduate School of Medicine, Osaka-sayama, Osaka, Japan.
Mucosal Immunol ; 9(5): 1234-49, 2016 09.
Article en En | MEDLINE | ID: mdl-26813347
Nucleotide-binding oligomerization domain 1 (NOD1) fulfills important host-defense functions via its responses to a variety of gut pathogens. Recently, however, we showed that in acute pancreatitis caused by administration of cholecystokinin receptor (CCKR) agonist (cerulein) NOD1 also has a role in inflammation via its responses to gut commensal organisms. In the present study, we explored the long-term outcome of such NOD1 responsiveness in a new model of chronic pancreatitis induced by repeated administration of low doses of cerulein in combination with NOD1 ligand. We found that the development of chronic pancreatitis in this model requires intact NOD1 and type I IFN signaling and that such signaling mediates a macrophage-mediated inflammatory response that supports interleukin (IL)-33 production by acinar cells. The IL-33, in turn, has a necessary role in the induction of IL-13 and TGF-ß1, factors causing the fibrotic reaction characteristic of chronic pancreatitis. Interestingly, the Th2 effects of IL-33 were attenuated by the concomitant type I IFN response since the inflammation was marked by clear increases in IFN-γ and TNF-α production but only marginal increases in IL-4 production. These studies establish chronic pancreatitis as an IL-33-dependent inflammation resulting from synergistic interactions between the NOD1 and CCKR signaling pathways.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Ceruletida / Receptores de Colecistoquinina / Ácido Diaminopimélico / Pancreatitis Crónica / Proteína Adaptadora de Señalización NOD1 / Interleucina-33 Tipo de estudio: Prognostic_studies Idioma: En Revista: Mucosal Immunol Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2016 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Ceruletida / Receptores de Colecistoquinina / Ácido Diaminopimélico / Pancreatitis Crónica / Proteína Adaptadora de Señalización NOD1 / Interleucina-33 Tipo de estudio: Prognostic_studies Idioma: En Revista: Mucosal Immunol Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2016 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos