Brandtzaeg Petter, van Deuren Marcel
Department of Pediatrics, Ullevål University Hospital, University of Oslo, Oslo, Norway.
Curr Opin Infect Dis. 2002 Jun;15(3):247-52. doi: 10.1097/00001432-200206000-00006.
Lipopolysaccharides in the outer membrane of Neisseria meningitidis are key molecules that induce inflammation and cause meningitis and shock. Mutant strains, with altered lipid A, the toxic moiety of lipopolysaccharide, or completely lacking lipopolysaccharide, induce significantly less inflammation than wild-type strains. Polymorphism of the Fc gamma receptors and interleukin-10 gene but not of the Toll-like receptor 4 may influence the development of meningococcal infection. Mannan-binding lectin is involved in complement activation, the regulation of adhesion molecules and cytokine production induced by meningococci. The activation of protein C by the thrombomodulin protein C receptor complex on the endothelial cell surface appears to be reduced in meningococcal sepsis but is still sufficient to convert protein C to activated protein C in patients treated with concentrated protein C.
脑膜炎奈瑟菌外膜中的脂多糖是诱导炎症并导致脑膜炎和休克的关键分子。脂质A（脂多糖的毒性部分）发生改变或完全缺乏脂多糖的突变菌株，其诱导的炎症明显少于野生型菌株。Fcγ受体和白细胞介素-10基因的多态性而非Toll样受体4的多态性可能会影响脑膜炎球菌感染的发展。甘露糖结合凝集素参与补体激活、脑膜炎球菌诱导的黏附分子调节和细胞因子产生。在内皮细胞表面，血栓调节蛋白蛋白C受体复合物对蛋白C的激活在脑膜炎球菌败血症中似乎有所减少，但在用浓缩蛋白C治疗的患者中，仍足以将蛋白C转化为活化蛋白C。
