Postbiotic cocktail attenuates DSS-induced colitis in mice via autophagy pathway modulation
Postbiotics from Limosilactobacillus spp. and Bifidobacterium spp. reduced experimental colitis markers and upregulated autophagy-related genes in mice.
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What the study showed
DSS-treated mice receiving postbiotics showed less body weight loss, longer colon length, and lower histopathological scores compared to the DSS-only group. Expression of autophagy genes (Atg5, Atg7, Atg12, Atg13, Beclin 1) was elevated in the postbiotic-treated group. Authors interpret these findings as evidence of autophagy-mediated anti-inflammatory regulation.
How it was done
Experimental study with 15 male C57BL/6 mice in three groups (control, DSS, DSS + postbiotics); postbiotics administered daily for 14 days at 1×10⁹ CFU/mL equivalent.
Risk of bias
Extremely small sample size (n=5 per group) and animal model limit generalizability; absence of a postbiotic-only group prevents assessment of intrinsic product effects. The abstract does not specify postbiotic composition or gene quantification methods.
What this study does NOT prove
This study does not prove efficacy, safety, or causal mechanism of postbiotics in human IBD.
In clinical practice
Findings are not transferable to humans at this stage. Evidence is insufficient for any clinical recommendation.
Limitations
Extremely small sample size (n=5 per group) and animal model limit generalizability; absence of a postbiotic-only group prevents assessment of intrinsic product effects. The abstract does not specify postbiotic composition or gene quantification methods.
Technical appendix
Version history
- 1.0 · 2026-08-25 — Auto-generated under Evidence Standard v1.0
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