Lack of mannose-binding lectin-A enhances survival in a mouse model of acute septic peritonitis

• Published in: Microbes and infection 2002-07, Vol.4 (8), p.773-784
• Main Authors: Takahashi, Kazue, Gordon, Judith, Liu, Hong, Sastry, Kedarnath N, Epstein, Judy E, Motwani, Monica, Laursen, Inga, Thiel, Steffen, Jensenius, Jens Christian, Carroll, Michael, Ezekowitz, R.Alan B
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; CLP; Disease Models, Animal; Fundamental and applied biological sciences. Psychology; Gene Deletion; IL-6; Inflammation; Inflammation - genetics; Inflammation - immunology; Interleukin-6 - analysis; Knockout; Leukocytes - immunology; Mannose-binding lectin (MBL); Mannose-Binding Lectin - analogs & derivatives; Mannose-Binding Lectin - deficiency; Mannose-Binding Lectin - genetics; Mannose-Binding Lectin - immunology; Mice; Mice, Knockout; Molecular and cellular biology; Peritonitis - genetics; Peritonitis - immunology; PMN; Septic shock; Stem Cells; Survival Analysis; TNF-α; Tumor Necrosis Factor-alpha - analysis
• ISSN: 1286-4579; 1769-714X
• DOI: 10.1016/S1286-4579(02)01597-6

The mannose-binding lectin (MBL) (also known as the mannose-binding protein) is a serum protein that plays a role as an “ante-antibody” in innate immunity. In man, MBL is encoded by a single gene, whereas in mice there are two homologous proteins, MBL-A and MBL-C. In order to evaluate the relative roles of these two forms of MBL, we created MBL-A null mice that were MBL-C sufficient. We found MBL-A null mice had enhanced survival in a septic peritonitis model compared to wild-type mice and complement 3 null mice at 24 h, 48 h and 10 d ( P