Answers are grounded in this paper and cite their sources.
Impairment of the intestinal epithelial barrier, accompanied by local and systemic inflammation, underlies numerous human pathologies, including inflammatory bowel diseases, celiac disease, sepsis, as well as severe acute malnutrition. Bifidobacterium longum subsp. infantis and Lacticaseibacillus rhamnosus GG (LGG®) have been shown in preclinical studies to strengthen the gut epithelial barrier and attenuate inflammation. This study aimed to compare the ability of four commercial strains of B. infantis, LGG, and their combination to mitigate inflammation-mediated epithelial damage using an in vitro immunocompetent intestinal model. A microfluidic mid-throughput platform OrganoPlate® was used to co-culture intestinal epithelial cells (Caco-2) with peripheral blood mononuclear cells (PBMCs). Epithelial damage was induced by stimulating PBMCs with lipopolysaccharide (LPS), and probiotic-conditioned media were applied to the apical side of Caco-2 cells to assess effects on barrier integrity, cytokine secretion, and gene transcription. All tested probiotics significantly protected the epithelium by modulating tight junction protein expression and promoting transcription of homeostatic cytokines, resulting in a “leak-tight” phenotype. These findings indicate that metabolites produced by B. infantis and/or LGG can protect the intestinal epithelium in vitro, warranting further in vivo studies to evaluate the translational relevance of this effect.
No takes yet. Share an insight, caveat, or question.
Belotserkovsky et al. (2025) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: