Fluid supplementation accelerates epithelial repair during chemical colitis.

Authors:
Ana M Santander
Ana M Santander
University of Miami Miller School of Medicine
Irina Fernandez
Irina Fernandez
The University of Texas at Austin
Ester Fernandez
Ester Fernandez
National Institutes of Health
United States
Julia Zaias
Julia Zaias
University of Miami Miller School of Medicine
United States
Maria T Abreu
Maria T Abreu
Mount Sinai School of Medicine
United States

PLoS One 2019 19;14(4):e0215387. Epub 2019 Apr 19.

Division of Gastroenterology, Department of Medicine, University of Miami-Leonard Miller School of Medicine, Miami, FL, United States of America.

The dextran sulfate sodium (DSS) model of colitis is a common animal model of inflammatory bowel disease that causes pain and distress. In this study, we aimed to determine whether fluid supplementation can be used as a welfare-based intervention to minimize animal suffering. C57Bl/6 females undergoing acute colitis by administration of 3% DSS in drinking water were supplemented with 1 mL intraperitoneal injections of NaCl and compared to non-supplemented control mice. Mouse behavior and locomotive activity were assessed on days 5-6 after DSS initiation by means of tail suspension, novel object recognition and open field activity tests. Mice were euthanized after either the acute (day 7) or the recovery phase (day 12) of colitis and inflammation, epithelial proliferation, and differentiation were assessed by means of histology, immunohistochemistry, quantitative PCR, and western blot. We found that fluid-supplemented mice had reduced signs of colitis with no alterations in behavior or locomotive activity. Furthermore, we observed an accelerated epithelial repair response after fluid hydration during the acute phase of colitis, characterized by increased crypt proliferation, activation of ERK1/2, and modulation of TGF-β1 expression. Consistent with these findings, fluid-supplemented mice had increased numbers of goblet cells, upregulated expression of differentiation markers for absorptive enterocytes, and reduced inflammation during the recovery phase. Our results show that fluid hydration does not reduce stress in DSS-treated mice but alters colitis evolution by reducing clinical signs and accelerating epithelial repair. These results argue against the routine use of fluid supplementation in DSS-treated mice.

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Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0215387PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6474653PMC
April 2019
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