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首页> 外文期刊>Infection and immunity >Involvement of C3a and C5a in Interleukin-8 Secretion by Human Polymorphonuclear Cells in Response to Capsular Material of Cryptococcus neoformans
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Involvement of C3a and C5a in Interleukin-8 Secretion by Human Polymorphonuclear Cells in Response to Capsular Material of Cryptococcus neoformans

机译：C3a和C5a参与人类多形核细胞对新型隐球菌荚膜物质的反应中白细胞介素8分泌。

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In a previous paper we demonstrated that human polymorphonuclear cells (PMN) in the presence of normal human serum (NHS) secrete proinflammatory cytokines in response to Cryptococcus neoformans or its major capsular component, glucuronoxylomannan (GXM). The hypothesis that activation of the complement system could be responsible for the observed phenomenon is supported by the fact that encapsulated and acapsular C. neoformans isolates are activators of the complement system and, in particular, large encapsulated isolates are powerful activators. In the present study we demonstrate that (i) interleukin-8 (IL-8) release in response to acapsular or encapsulated strains of C. neoformans is significantly reduced in the presence of heat-inactivated serum rather than NHS and is completely abrogated in the absence of human serum; (ii) GXM-induced IL-8 release is strictly dependent on the presence of NHS, is inhibited by specific antibodies to either C3a and C5 complement components, and is completely abrogated by the combined use of these antibodies; (iii) the addition of purified C3a and C5a directly stimulates IL-8 release by PMN; and (iv) monoclonal antibody to GXM in combination with GXM or encapsulated C. neoformans potentiates IL-8 release by PMN. These data shed light on the mechanism involved in GXM-induced IL-8 secretion by PMN, provide an additional potential role for complement in the control of C. neoformans infections, and suggest a complex interplay between the complement system, humoral immunity, and cytokine regulation.
机译：在先前的论文中，我们证明了在正常人血清（NHS）存在的情况下，人多形核细胞（PMN）分泌促炎细胞因子，以响应新型隐球菌或其主要荚膜成分葡糖醛酸羟甘露聚糖（GXM）。包裹的和包裹的 C事实支持了补体系统激活可能是所观察到的现象的假说。新福尔摩斯分离株是补体系统的激活剂，尤其是大包封的分离株是强大的激活剂。在本研究中，我们证明了（i）白细胞介素8（IL-8）的释放是针对C的包膜或包膜菌株。在存在热灭活的血清而不是NHS的情况下，新福尔摩斯显着减少，而在没有人血清的情况下，新福尔摩斯完全消失。 （ii）GXM诱导的IL-8释放严格取决于NHS的存在，被针对C3a和C5补体成分的特异性抗体抑制，并被这些抗体的联合使用完全废除; （iii）加入纯化的C3a和C5a直接刺激PMN释放IL-8; （iv）与GXM或包封的 C组合的针对GXM的单克隆抗体。新甲虫增强PMN释放IL-8。这些数据阐明了PMN参与GXM诱导的IL-8分泌的机制，为补体在 C的控制中提供了额外的潜在作用。感染，提示补体系统，体液免疫和细胞因子调节之间存在复杂的相互作用。

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