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Talà, Adelfia; Guerra, Flora; Resta, Silvia Caterina; Calcagnile, Matteo; Barca, Amilcare; Tredici, Salvatore Maurizio; De Donno, Maria Dolores; Vacca, Mirco; Liso, Marina; Chieppa, Marcello; De Angelis, Maria; Verri, Tiziano; Bozzetti, Maria Giuseppina; Bucci, Cecilia; Alifano, Pietro

Phenotyping of Fecal Microbiota of Winnie, a Rodent Model of Spontaneous Chronic Colitis, Reveals Specific Metabolic, Genotoxic, and Pro-inflammatory Properties

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  • Media type: E-Article
  • Title: Phenotyping of Fecal Microbiota of Winnie, a Rodent Model of Spontaneous Chronic Colitis, Reveals Specific Metabolic, Genotoxic, and Pro-inflammatory Properties
  • Contributor: Talà, Adelfia; Guerra, Flora; Resta, Silvia Caterina; Calcagnile, Matteo; Barca, Amilcare; Tredici, Salvatore Maurizio; De Donno, Maria Dolores; Vacca, Mirco; Liso, Marina; Chieppa, Marcello; De Angelis, Maria; Verri, Tiziano; Bozzetti, Maria Giuseppina; Bucci, Cecilia; Alifano, Pietro
  • imprint: Springer Science and Business Media LLC, 2022
  • Published in: Inflammation
  • Language: English
  • DOI: 10.1007/s10753-022-01706-0
  • ISSN: 1573-2576; 0360-3997
  • Keywords: Immunology ; Immunology and Allergy
  • Origination:
  • Footnote:
  • Description: <jats:title> <jats:italic>Abstract</jats:italic> </jats:title><jats:p><jats:italic>Winnie</jats:italic>, a mouse carrying a missense mutation in the <jats:italic>MUC2</jats:italic> mucin gene, is a valuable model for inflammatory bowel disease (IBD) with signs and symptoms that have multiple similarities with those observed in patients with ulcerative colitis. MUC2 mucin is present in <jats:italic>Winnie</jats:italic>, but is not firmly compacted in a tight inner layer. Indeed, these mice develop chronic intestinal inflammation due to the primary epithelial defect with signs of mucosal damage, including thickening of muscle and mucosal layers, goblet cell loss, increased intestinal permeability, enhanced susceptibility to luminal inflammation-inducing toxins, and alteration of innervation in the distal colon. In this study, we show that the intestinal environment of the <jats:italic>Winnie</jats:italic> mouse, genetically determined by <jats:italic>MUC2</jats:italic> mutation, selects an intestinal microbial community characterized by specific pro-inflammatory, genotoxic, and metabolic features that could imply a direct involvement in the pathogenesis of chronic intestinal inflammation. We report results obtained by using a variety of in vitro approaches for fecal microbiota functional characterization. These approaches include Caco-2 cell cultures and Caco-2/THP-1 cell co-culture models for evaluation of geno-cytotoxic and pro-inflammatory properties using a panel of 43 marker RNAs assayed by RT-qPCR, and cell-based phenotypic testing for metabolic profiling of the intestinal microbial communities by Biolog EcoPlates. While adding a further step towards understanding the etiopathogenetic mechanisms underlying IBD, the results of this study provide a reliable method for phenotyping gut microbial communities, which can complement their structural characterization by providing novel functional information. </jats:p>