Mouse mannose-binding lectin-A and ficolin-A inhibit lipopolysaccharide-mediated pro-inflammatory responses on mast cells

• Published in: BMB reports 2013, 46(7), , pp.376-381
• Main Authors: Ma, Y.J., Pusan National University, Busan, Republic of Korea, Kang, H.J., Hallym University College of Medicine, Anyang, Republic of Korea, Kim, J.Y., Hallym University College of Medicine, Anyang, Republic of Korea, Garred, P., University of Copenhagen, Copenhagen, Denmark, Lee, M.S., Sungkyunkwan University School of Medicine, Seoul, Republic of Korea, Lee, B.L., Pusan National University, Busan, Republic of Korea
• Format: Article
• Language: English
• Subjects: CELULAS FIBROSAS; Ficolin; Ficolin,Innate immunity,Mannose-binding lectin,Toll-like receptor; Innate immunity; Mannose-binding lectin; Mast cell; MAST CELLS; MASTOCYTE; Toll-like receptor; 화학
• ISSN: 1976-6696; 1976-670X
• DOI: 10.5483/BMBRep.2013.46.7.055

blood, such as mannose-binding lectin (MBL) and ficolins, modulate mast cell-mediated inflammatory responses. We investigate how mouse MBL-A or ficolin-A regulate mouse bone marrow-derived mast cells (mBMMCs)-derived inflammatory response against bacterial lipopolysaccharide (LPS) stimulation. LPS-mediated pro-inflammatory cytokine productions on mBMMCs obtained from Toll-like receptor4 (TLR4)-deficient mice, TLR2-defficient mice, and their wildtype, were specifically attenuated by the addition of either mouse MBL-A or ficolin-A in a dose-dependent manner. However, the inhibitory effects by mouse MBL-A or ficolin-A were restored by the addition of mannose or N-acetylglucosamine, respectively. These results suggest that mouse MBL-A and ficolin-A bind to LPS via its carbohydrate-recognition domain and fibrinogen-like domain, respectively, whereby cytokine production by LPSmediated TLR4 in mBMMCs appears to be down-regulated, indicating that mouse MBL and ficolin may have an inhibitory function toward mouse TLR4-mediated excessive inflammation on the mast cells.