the human host defense peptide ll-37 interacts with neisseria meningitidis capsular polysaccharides and inhibits inflammatory mediators release人类宿主防御肽ll-37与脑膜炎奈瑟菌荚膜多糖,抑制炎症介质释放.pdfVIP

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the human host defense peptide ll-37 interacts with neisseria meningitidis capsular polysaccharides and inhibits inflammatory mediators release人类宿主防御肽ll-37与脑膜炎奈瑟菌荚膜多糖,抑制炎症介质释放.pdf

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the human host defense peptide ll-37 interacts with neisseria meningitidis capsular polysaccharides and inhibits inflammatory mediators release人类宿主防御肽ll-37与脑膜炎奈瑟菌荚膜多糖,抑制炎症介质释放

The Human Host Defense Peptide LL-37 Interacts with Neisseria meningitidis Capsular Polysaccharides and Inhibits Inflammatory Mediators Release 1 2¤ 2¤ 1,3,4 3,4 Susu M. Zughaier *, Pavel Svoboda , Jan Pohl , David S. Stephens , William M. Shafer 1 Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine and Laboratories of Microbial Pathogenesis, Atlanta, Georgia, United States of America, 2 Microchemical and Proteomics Facility, Emory University School of Medicine and Laboratories of Microbial Pathogenesis, Atlanta, Georgia, United States of America, 3 Department of Microbiology and Immunology, Emory University School of Medicine and Laboratories of Microbial Pathogenesis, Atlanta, Georgia, United States of America, 4 Department of Veterans Affairs Medical Center, Atlanta, Georgia, United States of America Abstract Capsular polysaccharides (CPS) are a major virulence factor in meningococcal infections and form the basis for serogroup designation and protective vaccines. Our work has identified meningococcal CPS as a pro-inflammatory ligand that functions through TLR2 and TLR4-MD2-dependent activation. We hypothesized that human cationic host defense peptides interact with CPS and influence its biologic activity. Accordingly, the interaction of meningococcal CPS with the human- derived cationic peptide LL-37, which is expressed by phagocytic and epithelial cells that interface with meningococci during infection, was investigated. LL-37 neutralized the pro-inflammatory activity of endotoxin-free CPS as assessed by TLR2 and TLR4-MD-2-dependent release of TNFa, IL-6 and IL-8 from human and murine macrophages.