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L-Ficolin and Capsular Polysaccharide-Specific IgG in Cord Serum Contribute Synergistically to Opsonophagocytic Killing of Serotype III and V Group B Streptococci

机译:脐带血清中的L-Ficolin和荚膜多糖特异性IgG协同作用于III型和V型B组链球菌的调理吞噬作用。

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Group B streptococci (GBS; Streptococcus agalactiae) are the most common cause of neonatal sepsis and meningitis. Serotype-specific IgG antibody is known to protect neonates against GBS infections by promoting opsonophagocytosis. The L-ficolin-mediated lectin pathway of the complement is also a potential mechanism for opsonization of GBS, because L-ficolin activates the complement after binding to serotype Ib, III, V, VI, and VIII GBS. In the present study, we investigated how L-ficolin and serotype-specific IgG in cord sera contribute to opsonophagocytic killing of GBS. Neither L-ficolin nor serotype-specific IgG concentrations correlated with C3b deposition on serotype Ib and VI GBS, suggesting L-ficolin- and serotype-specific IgG-independent mechanisms of complement activation. The percentage of serotype VIII GBS killed was high regardless of the concentration of L-ficolin and IgG. In contrast, L-ficolin and serotype-specific IgG can each initiate C3b deposition on serotype III and V GBS and promote phagocytosis by polymorphonuclear leukocytes, but L-ficolin and serotype-specific IgG together promote opsonophagocytic killing to a greater extent than does either alone in vitro. This synergy was observed when serotype III-specific IgG concentrations were between 1 and 6 μg/ml and when serotype V-specific IgG concentrations were between 2 and 5 μg/ml. Concentrations of serotype III-specific IgG in cord blood above 7 μg/ml are considered protective for neonates colonized with GBS, but most neonates with IgG levels of less than 7 μg/ml do not develop GBS infections. The data presented here suggest that L-ficolin enhances opsonophagocytosis of serotype III and V GBS when serotype-specific IgG alone is suboptimal for protection.
机译:B组链球菌(GBS;无乳链球菌)是新生儿败血症和脑膜炎的最常见原因。已知血清型特异性IgG抗体通过促进调理吞噬作用来保护新生儿免受GBS感染。补体的L-纤维胶凝蛋白介导的凝集素途径也是GBS调理作用的潜在机制,因为L-纤维胶凝蛋白结合血清型Ib,III,V,VI和VIII GBS后会激活补体。在本研究中,我们研究了脐带血清中的L-纤维胶凝蛋白和血清型特异性IgG如何促成GBS的调理吞噬作用。 L-丝胶蛋白或血清型特异性IgG浓度均与C3b在Ib型和VI GBS血清型上的沉积无关,提示L-丝胶蛋白和血清型特异性IgG独立的补体激活机制。不论L-纤维胶凝素和IgG的浓度如何,被杀死的VIII型血清型GBS的百分比都很高。相比之下,L-纤维胶凝蛋白和血清型特异性IgG可以各自在III型和V GBS血清上引发C3b沉积并促进多形核白细胞的吞噬作用,但是与单独使用L-纤维胶蛋白和血清型特异性IgG相比,它们在更大程度上促进调理吞噬细胞的杀伤作用。 体外。当血清型III特异性IgG浓度在1-6μg/ ml之间和当血清型V特异性IgG浓度在2至5μg/ ml之间时,观察到这种协同作用。脐带血中浓度高于7μg/ ml的血清型III特异性IgG浓度被认为对GBS定植的新生儿具有保护作用,但大多数IgG水平低于7μg/ ml的新生儿不会发展为GBS感染。此处提供的数据表明,当单独的血清型特异性IgG对保护作用不理想时,L-纤维胶凝蛋白会增强III型和V GBS血清的调理吞噬作用。

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