Anti-inflammatory Activity and Mechanism of Surfactin in Lipopolysaccharide-Activated Macrophages

• Published in: Inflammation 2015-04, Vol.38 (2), p.756-764
• Main Authors: Zhang, Yuanyuan, Liu, Chuan, Dong, Bin, Ma, Xiaolei, Hou, Lihua, Cao, Xiaohong, Wang, Chunling
• Format: Article
• Language: English
• Subjects: Animals; Anti-Inflammatory Agents - pharmacology; Bacillus natto; Biomedical and Life Sciences; Biomedicine; Cell Survival - drug effects; Cell Survival - physiology; Dose-Response Relationship, Drug; Immunology; Inflammation Mediators - antagonists & inhibitors; Inflammation Mediators - metabolism; Internal Medicine; Lipopeptides - pharmacology; Lipopolysaccharides - toxicity; Macrophages - drug effects; Macrophages - metabolism; Mice; Pathology; Peptides, Cyclic - pharmacology; Pharmacology/Toxicology; Rheumatology
• ISSN: 0360-3997; 1573-2576
• DOI: 10.1007/s10753-014-9986-y

Surfactin is primarily produced by Bacillus natto TK-1 and is one of the most powerful biosurfactants. It consists of a heptapeptide interlinked with a β-hydroxy fatty acid. Because of its special structure, surfactin shows broad biological effects, including anti-tumour, anti-microbial and anti-mycoplasma activities. It also has potential anti-inflammatory activity; however, the anti-inflammatory mechanism of surfactin has not been explored. In this study, we investigated the anti-inflammatory mechanism of surfactin in lipopolysaccharide (LPS)-stimulated macrophages. Surfactin exhibited an anti-inflammatory effect without cytotoxicity at certain concentrations, and the lipopolysaccharide (LPS)-stimulated cells appeared normal after surfactin treatment. Surfactin significantly inhibited the increased expression of IFN-γ, IL-6, iNOS and nitric oxide (NO). TLR4 is the critical receptor for LPS; therefore, the TLR4 signal transduction pathway is the primary pathway that mediates LPS-induced inflammation. The results show that surfactin downregulated the LPS-induced TLR4 protein expression of macrophages and indicated that the surfactin-mediated signal pathway was involved in with TLR4. The subsequent studies demonstrated that surfactin exhibited anti-inflammatory effects by attenuating the activation of nuclear factor-κB (NF-κB), which is involved in the nuclear factor-κB (NF-κB) cell signalling pathways. These results suggest that surfactin may be a new therapeutic agent for inflammation.