Abstract
Lactoferrin (LF) plays an essential immunomodulatory role, yet its underlying mechanisms remain unclear. Here, we investigated the suppressive effects of bovine LF and its peptide derivatives (at positions 17–28 of the primary structure) on ulcerative colitis (UC) using a dextran sodium sulphate (DSS)-induced UC mouse model. LF peptides and their amide bodies alleviated DSS-induced colon atrophy. Mice orally administered with LF and its peptides showed decreased epithelial tissue collapse and preserved crypt structure. Additionally, measurement of lipopolysaccharide (LPS) -induced inflammatory cytokine levels in cell culture systems, using macrophage-like RAW264.7, neutrophil-like HL-60, and intestinal epithelium-like Caco-2 cells, suggested the anti-inflammatory effect of LF peptides on intestinal immune function as a possible mechanism underlying LF-induced suppression of UC onset. Thus, LF peptide derivatives may be useful for treating some inflammatory diseases, as the modulatory effect of LF peptide and its amide body was more effective than that of LF.
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