Stress is the body’s coordinated response to stimuli that threaten its internal stability. It is a risk factor that alters the functionality of the gastrointestinal tract. This study evaluated the effect of Lactiplantibacillus plantarum 299v on chronic stress-induced morphological alterations in the small and large intestine, the expression of intestinal barrier and immune related genes, and gut microbiota composition in 52-day old male Wistar rats. The animals were randomly assigned to three groups: control (C), chronic restraint stress (S), and chronic restraint stress plus L. plantarum (1 × 1010 CFU/mL, SP). The chronic restraint stress protocol consisted of a 1-h daily session, 5 days per week, for four consecutive weeks. Administration of L. plantarum increased the number of goblet cells in the duodenum, ileum, and colon, reduced villus width in the duodenum, and enhanced villus length in the duodenum and jejunum. In terms of gene expression, occludin (OCLN) was upregulated in the duodenum of the S group, while both OCLN and superoxide dismutase (SOD) were downregulated in the jejunum of the SP group. In the ileum, interleukin-10 (IL10), claudin-1 (CLDN1), and mucin-2 (MUC2) were upregulated, whereas SOD was downregulated in the SP group. Moreover, L. plantarum supplementation modulated gut microbial community structure by reducing the abundance of opportunistic pathogens such as Alloprevotella and Treponema. In conclusion, L. plantarum 299v exerts protective effects against chronic stress by preserving intestinal barrier integrity, enhancing mucosal immune response, and attenuating stress-induced gastrointestinal damage in young male rats.
Lactiplantibacillus plantarum Intake Reduces Gastrointestinal Tract Damage Caused by Chronic Stress in Young Rats
D. C. Castro-Rodríguez,E. Pérez-Sánchez,Georgina Hernández-Montes,Julián Fernando Oviedo-León,L. Nicolás-Toledo
Published 2025 in ACS Omega
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- Publication year
2025
- Venue
ACS Omega
- Publication date
2025-11-09
- Fields of study
Biology, Medicine, Environmental Science
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- Source metadata
Semantic Scholar, PubMed
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