Comparative Effects of Probiotics and Paraprobiotics Derived from Lactiplantibacillus plantarum, Latilactobacillus sakei, and Limosilactobacillus reuteri in a DSS-Induced Ulcerative Colitis Mouse Model.

Abstract

Live biotherapeutic products, represented by probiotics with disease-mitigating or therapeutic effects, face significant limitations in achieving stable colonization in the gut through oral administration. However, paraprobiotics, which consist of dead or inactivated microbial cells derived from probiotics, can provide comparable health benefits while overcoming the limitations associated with live biotherapeutic products. Therefore, the purpose of this study was to quantitatively compare and analyze the effects of probiotics, which are gaining attention as treatments for inflammatory bowel diseases, and their paraprobiotic counterparts on the alleviation of ulcerative colitis. In in vitro evaluations revealed that the paraprobiotics derived from Lactiplantibacillus plantarum MGEL20154, Latilactobacillus sakei MGEL23040, and Limosilactobacillus reuteri MGEL21001 exhibited equal or significantly enhanced activities in terms of antioxidant properties, anti-inflammatory effects, and barrier integrity enhancement compared to their probiotic counterparts. Furthermore, consistent with in vitro findings, both probiotics and paraprobiotics effectively improved histological scores and reduced myeloperoxidase levels in a DSS-induced ulcerative colitis mouse model. Notably, paraprobiotics derived from L. plantarum MGEL20154 and L. reuteri MGEL21001 demonstrated significantly enhanced efficacy in restoring tight junctions, promoting mucin secretion, and reducing inflammation in colonic lesion tissues compared to their probiotic forms. Our results suggest that these paraprobiotics may serve as more suitable agents for alleviating and treating ulcerative colitis, addressing limitations associated with probiotics, such as low survival rates, instability, antibiotic susceptibility, and the potential induction of excessive inflammatory responses.