Anti-inflammatory effects of heat-killed Lactiplantibacillus argentoratensis BBLB001 on a gut inflammation co-culture cell model and dextran sulfate sodium-induced colitis mouse model.

Dysbiosis caused by dietary changes can alter the intestinal bacterial species and is closely associated with inflammatory bowel disease (IBD). Among the possible treatment options, postbiotics, which act to balance the constituent intestinal microflora, have gained substantial attention. Herein, we investigated the anti-inflammatory effects of heat-killed Lactiplantibacillus argentoratensis (hk-LA) BBLB001 isolated from a marine environment using both cell (Caco2/RAW264.7 cell co-culture) and animal (dextran sodium sulfate [DSS]-induced colitis in mice) models. hk-LA BBLB001 markedly reduced IL-8 secretion in Caco-2 cell culture medium after lipopolysaccharide-mediated stimulation of RAW264.7 cells by enhancing the expression of cell adhesion factors.The body weight loss, reduced inflammatory cytokine levels in the serum and colon tissues, colon shortening, and myeloperoxidase activation caused by DSS in mice were alleviated by hk-LA BBLB001. Similar to that in the intestinal cell model, the gene and protein expressions of cell adhesion molecules in the colon tissue were increased upon hk-LA BBLB001 treatment in DSS-induced colitis mice. We observed increased mucin expression and secretory IgA concentration in colon tissues, suggesting that hk-LA BBLB001 intake may benefit pathogen defense and the regulation of intestinal commensal bacteria. Thus, hk-LA BBLB001 may serve as an instrumental postbiotic material in IBD treatment.