The abstract is read at the publisher; the summary is JClub's.
Heat-killed Latilactobacillus sakei D279 attenuates LPS-induced intestinal injury in LPS-challenged mice, reducing colon shortening and histopathological damage versus LPS controls.
- Why it matters: Intestinal barrier dysfunction and excessive inflammation drive metabolic and gastrointestinal disease, and it is unclear whether this heat-killed probiotic can protect gut integrity during systemic inflammatory stress.
- What they did: Mice were challenged with LPS and treated with heat-killed D279; macrophage inflammatory signaling was tested ex vivo by measuring cytokine and receptor gene expression, and barrier effects were assessed in IEC-6 cells using TEER and tight junction gene expression.
- The result: D279 suppressed LPS-induced pro-inflammatory cytokine gene expression (TNF-, IL-1{beta}, IL-12{beta}), increased IL-10, reduced LPS-driven MLCK upregulation, improved IEC-6 viability, increased TEER, and upregulated tight junction genes.
The findingWhy it mattersWhat they didThe result
AI summary of the abstract · may contain errors · not medical advice · read the paper.