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Konjac Glucomannan Oligosaccharides Prevent Intestinal Inflammation Through SIGNR1-Mediated Regulation of Alternatively Activated Macrophages.
Tang, Jiqing; Liu, Jun; Yan, Qiaojuan; Gu, Zhenglong; August, Avery; Huang, Weishan; Jiang, Zhengqiang.
Afiliación
  • Tang J; Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, 100083, China.
  • Liu J; Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, 100083, China.
  • Yan Q; Key Laboratory of Food Bioengineering (China National Light Industry), College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, 100083, China.
  • Gu Z; Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, 100083, China.
  • August A; Division of Nutritional Sciences, Cornell University, Ithaca, NY, 14853, USA.
  • Huang W; Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, 13843, USA.
  • Jiang Z; Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, 13843, USA.
Mol Nutr Food Res ; 65(20): e2001010, 2021 10.
Article en En | MEDLINE | ID: mdl-34390195
SCOPE: Konjac glucomannan oligosaccharides (KMOS) are prebiotics and may improve intestinal immunity through modulation of macrophage function. However, the underlying molecular mechanisms were unclear. METHODS AND RESULTS: Using a mouse model of dextran sulfated sodium (DSS)-induced acute colitis, the study demonstrates here that KMOS (400 mg-1 kg-1 d-1 ) can ameliorate intestinal inflammation in a macrophage dependent manner. Oral exposure to KMOS prevents DSS-induced intestinal pathology, improves epithelial integrity, and decreases accumulation of colonic inflammatory leukocytes and cytokines. The therapeutic effects of KMOS are dependent on the function of macrophages, as depletion of macrophages abolished the effects. In colonic lamina propria of DSS-treated mice, as well as in vitro culture of bone marrow derived macrophages (BMDMs), KMOS skews reprogramming of classically activated macrophages (CAM/M1) into alternatively activated macrophages (AAM/M2). The study further determines that the activation of SIGNR1/phospho-c-Raf (S338)/phospho-p65 (S276)/acetyl-p65 (K310) pathway is responsible for KMOS-induced AAM/M2 polarization. Blockage of SIGNR1 abolishes KMOS-induced AAM/M2 polarization of activated macrophages, expression of phospho-p65 (S276) in colonic macrophages, and alleviation of DSS-induced colitis in mice, suggesting that SIGNR1 is critical for macrophage responses to KMOS. CONCLUSIONS: This study reveals a SIGNR1-mediated macrophage-dependent pathway that supports regulatory function of KMOS in host immunity and intestinal homeostasis.
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Texto completo: 1 Base de datos: MEDLINE Asunto principal: Oligosacáridos / Moléculas de Adhesión Celular / Colitis / Receptores de Superficie Celular / Lectinas Tipo C / Prebióticos / Activación de Macrófagos / Mananos Idioma: En Revista: Mol Nutr Food Res Asunto de la revista: CIENCIAS DA NUTRICAO Año: 2021 Tipo del documento: Article

Texto completo: 1 Base de datos: MEDLINE Asunto principal: Oligosacáridos / Moléculas de Adhesión Celular / Colitis / Receptores de Superficie Celular / Lectinas Tipo C / Prebióticos / Activación de Macrófagos / Mananos Idioma: En Revista: Mol Nutr Food Res Asunto de la revista: CIENCIAS DA NUTRICAO Año: 2021 Tipo del documento: Article