1. Colonic Lesions, Cytokine Profiles, and Gut Microbiota in Plasminogen-Deficient Mice.
- Author
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Vestergaard B, Krych Ł, Lund LR, Jørgensen BP, Hansen L, Jensen HE, Nielsen DS, and Hansen AK
- Subjects
- Animals, Colitis genetics, Colitis microbiology, Colitis pathology, Colon microbiology, Colon pathology, Feces microbiology, Genetic Predisposition to Disease, Male, Mice, 129 Strain, Mice, Knockout, Necrosis, Phenotype, Plasminogen genetics, Rectal Prolapse genetics, Rectal Prolapse microbiology, Rectal Prolapse pathology, Time Factors, Wound Healing, Colitis metabolism, Colon metabolism, Cytokines metabolism, Gastrointestinal Microbiome, Inflammation Mediators metabolism, Plasminogen deficiency, Rectal Prolapse metabolism
- Abstract
Plasminogen-deficient (FVB/NPan-plg(tm1Jld), plg(tm1Jld)) mice, which are widely used as a wound-healing model, are prone to spontaneous rectal prolapses. The aims of this study were 1) to evaluate the fecal microbiome of plg(tm1Jld) mice for features that might contribute to the development of rectal prolapses and colonic inflammation and 2) to assess the relevance of the inflammatory phenotype to the variability in wound healing in this model. The (plgtm1Jld) mice exhibited delayed wound healing, and they could be divided into 3 distinct groups that differed according to the time until wound closure. Colonic lesions in plg(tm1Jld) mice, which were characterized by necrotizing ulcerations and cystically dilated glands, were restricted to the intermediate and distal parts of the colon. The cytokine profile was indicative of chronic tissue damage, but the genetic modification did not change the composition of the gut microbiota, and none of the clinical or biochemical parameters correlated with the gut microbiota composition.
- Published
- 2015