LFP-20, a porcine lactoferrin peptide, ameliorates LPS-induced inflammation via the MyD88/NF-κB and MyD88/MAPK signaling pathways. Issue 2 (October 2015)

• Record Type: Journal Article
• Authors: Zong, Xin; Song, Deguang; Wang, Tenghao; Xia, Xi; Hu, Wangyang; Han, Feifei; Wang, Yizhen
• Is Part Of: Developmental and comparative immunology. Volume 52:Issue 2(2015)
• Page Start: 123
• Page End: 131
• Publication Date: 2015-10
• Subjects: LFP-20 -- Lipopolysaccharide -- Inflammation -- MyD88 -- NF-κB -- MAPK; Immunology -- Periodicals; Developmental immunology -- Periodicals; 616.079
• DOI: 10.1016/j.dci.2015.05.006
• Languages: English
• ISSNs: 0145-305X

Abstract

Highlights: LFP-20 suppressed the production of the pro-inflammatory cytokines in vitro and in vivo . LFP-20 affects LPS-induced cytokine production independently of its LPS-binding activity. Inhibitory effects of LFP-20 on production of pro-inflammatory cytokines associated with NF-κB and MAPK signaling. LFP-20 may directly influence MyD88 levels to block its interactions with NF-κB and MAPKs signaling molecules. Abstract: LFP-20 is one of the 20 amino acid anti-microbial peptides identified in the N terminus of porcine lactoferrin. Apart from its extensively studied direct anti-bacterial activity, its potential as an activator of immune-related cellular functions is unknown. Therefore, this study investigated its anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated pig alveolar macrophages in vitro and systemic inflammation in an in vivo mouse model. We found that the inhibitory effects of LFP-20 on production of pro-inflammatory cytokines were independent of its LPS-binding activity. However, they were associated with NF-κB and MAPK-dependent signaling. Furthermore, LFP-20 might directly influence MyD88 levels to block its interaction with NF-κB and MAPK-dependent signaling molecules that might alter LPS-mediated inflammatory responses in activated macrophages. Taken together, our data indicated that LFP-20 prevents the LPS-induced inflammatory response by inhibiting MyD88/NF-κB and MyD88/MAPK signaling pathways, and sheds light on the potential use of LFP-20 in the therapy of LPS-mediated sepsis.