OM85 ameliorates bleomycin-induced pulmonary fibrosis in mice by inhibiting Notch expression and modulating the IFN-γ/IL-4 ratio.

ABSTRACT: Th1/Th2 balances may play a vital role in the processes of inflammation and fibrosis. The Th1/Th2 paradigm can be evaluated by representing IFN-γ for Th1 and IL-4 for Th2. OM-85 BV encouraged preferential development of the Th1-type immunity characterized by amplified IFN-γ and decreased IL-4 production. This study aimed to evaluate the inhibitory effect of OM85 on bleomycin (BLM)-induced pulmonary fibrosis in C57 and its possible mechanisms. In vitro experiments demonstrated that OM85 exhibited no significant toxicity to HELF cells. OM-85 inhibited the TGF-β1-induced protein expression of Notch1 and Hes1 and reduced the fibrosis-related marker profiles, such as collagen I, collagen III, fibronectin, P21, and α-SMA, following TGF-β1 treatment of these cells. Immunofluorescence also reveale

SUBMITTER: Yu Y 

PROVIDER: S-EPMC11825818 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature