Clostridioides difficile infection promotes gastrointestinal dysfunction in human and mice post-acute phase of the disease.

Autor: Costa DVS; Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, VA, USA. Electronic address: deiziane2009@gmail.com., Pham N; Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, VA, USA., Loureiro AV; Department of Morphology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Ceará, Brazil., Yang SE; Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, VA, USA., Behm BW; Division of Gastroenterology and Hepatology, University of Virginia, Charlottesville, VA, USA., Warren CA; Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, VA, USA. Electronic address: ca6t@virginia.edu.
Jazyk: angličtina
Zdroj: Anaerobe [Anaerobe] 2024 Jun; Vol. 87, pp. 102837. Date of Electronic Publication: 2024 Mar 26.
DOI: 10.1016/j.anaerobe.2024.102837
Abstrakt: Objectives: In the US, Clostridioides difficile (C. difficile) infection (CDI) is the 8th leading cause of hospital readmission and 7th for mortality among all gastrointestinal (GI) disorders. Here, we investigated GI dysfunction post-CDI in humans and mice post-acute infection.
Materials and Methods: From March 2020 to July 2021, we reviewed the clinical records of 67 patients referred to the UVA Complicated C. difficile clinic for fecal microbiota transplantation (FMT) eligibility. C57BL/6 mice were infected with C. difficile and clinical scores were determined daily. Stool samples from mice were collected to measure the shedding of C. difficile and myeloperoxidase (MPO) levels. On day 21 post-infection, Evans's blue and FITC-70kDa methods were performed to evaluate GI motility in mice.
Results: Of the 67 patients evaluated at the C. difficile clinic, 40 patients (59.7%) were confirmed to have CDI, and 22 patients (32.8%) with post-CDI IBS (diarrhea-type, constipation-type, and mixed-type). In infected mice, levels of MPO in stools and clinical score were higher on day 3. On day 21, mice recovered from body weight loss induced by CDI, and fecal MPO was undetectable. The total GI transit time (TGITT) and FITC-70kDa levels on the proximal colon were increased in infected mice (p = 0.002), suggesting a constipation phenotype post-acute phase of CDI. A positive correlation intestinal inflammation on day 3 and TGITT on day 21 was observed.
Conclusion: In conclusion, post-infection intestinal dysfunction occurs in humans and mice post-CDI. Importantly, we have validated in the mouse model that CDI causes abnormal GI transit in the recovery phase of the disease, indicating the potential utility of the model in exploring the underlying mechanisms of post-infectious IBS in humans.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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