<em>Bifidobacterium longum</em> subsp. <em>infantis</em> and <em>Lacticaseibacillus rhamnosus</em> GG Protect Intestinal Epithelium Against Inflammation-Mediated Damage in an Immunocompetent<em> In-Vitro</em> Model

Severe acute malnutrition is associated with enteropathy manifested as disruption of epithelial tight junctions and increased gut permeability, associated with intestinal and systemic inflammation. Bifidobacterium longum subsp. infantis (B. infantis) and Lacticaseibacillus rhamnosus GG (LGG ®, Chr. Hansen A/S) have been shown to strengthen the gut epithelial barrier and to reduce inflammation in preclinical studies. The aim of this study was 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 model of the intestine. A microfluidic mid-throughput device OrganoPlate® (Mimetas B.V.) was employed to enable the co-culturing of intestinal epithelial cells (Caco-2) with peripheral blood mononuclear cells. Epithelial damage was induced by stimulating PBMCs with lipopolysaccharide and probiotic conditioned media were added to the apical side of the Caco-2 to test the effects on barrier integrity, cytokine secretion, and gene transcription. All tested probiotics demonstrated significant protection of the epithelium via modulation of tight-junction proteins and homeostatic cytokines gene transcription promoting a “leak-tight” phenotype. These findings demonstrate that B. infantis and/or LGG may have the potential to protect the intestinal epithelium and thus could contribute to alleviating intestinal enteropathy in malnourished children.