ReviewProbiotics and antimicrobial proteins2026
Role of Probiotics in Colitis Management: Mechanisms and Therapeutic Potential from Animal Studies.
Review in Probiotics and antimicrobial proteins, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
3 authors.
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Abstract
This review examines the therapeutic potential of probiotics in alleviating colitis through animal model studies, with particular emphasis on elucidating their mechanisms of action. Growing evidence demonstrates that gut dysbiosis plays a significant role in colitis pathophysiology, and restoring gut homeostasis represents a promising treatment strategy. Recent findings reveal that intestinal homeostasis is regulated not only by microbial composition but also by host-mediated oxygen control, which critically influences intestinal epithelial energy metabolism in both healthy and dysbiotic states. Interventional animal studies demonstrate that probiotics and their metabolites maintain gut homeostasis through multiple mechanisms. These include enhancing intestinal barrier integrity, preserving mucosal barrier function, and suppressing NF-κB pathway activation. Probiotics also modulate inflammatory responses by reducing pro-inflammatory cytokines such as TNF-α, IL-1β, IL-18, IL-6, and IL-17, while increasing anti-inflammatory cytokines like IL-10 and IL-13. Furthermore, they regulate macrophage polarization by downregulating M1 (pro-inflammatory) and upregulating M2 (anti-inflammatory) phenotypes. Additionally, probiotics ameliorate oxidative stress by boosting antioxidant enzyme activity (SOD, CAT, GPx, GST), increasing glutathione (GSH) levels, and decreasing MPO and MDA concentrations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.