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http://dx.doi.org/10.5483/BMBRep.2013.46.7.055

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

Ma, Ying Jie (The Global Research Laboratory of Insect Symbiosis, College of Pharmacy, Pusan National University)
Kang, Hee Jung (Department of Laboratory Medicine, Hallym University College of Medicine)
Kim, Ji Yeon (Department of Laboratory Medicine, Hallym University College of Medicine)
Garred, Peter (Laboratory of Molecular Medicine, Department of Clinical Immunology)
Lee, Myung-Shik (Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine)
Lee, Bok Luel (The Global Research Laboratory of Insect Symbiosis, College of Pharmacy, Pusan National University)
Publication Information
BMB Reports / v.46, no.7, 2013 , pp. 376-381 More about this Journal
Abstract
It is unknown how soluble pattern-recognition receptors in 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 LPS-mediated 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.
Keywords
Ficolin; Innate immunity; Mannose-binding lectin; Mast cell; Toll-like receptor;
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