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首页> 外文期刊>Infection and immunity >A Serotype 3 Pneumococcal Capsular Polysaccharide-Specific Monoclonal Antibody Requires Fcγ Receptor III and Macrophages To Mediate Protection against Pneumococcal Pneumonia in Mice
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A Serotype 3 Pneumococcal Capsular Polysaccharide-Specific Monoclonal Antibody Requires Fcγ Receptor III and Macrophages To Mediate Protection against Pneumococcal Pneumonia in Mice

机译：血清型3肺炎球菌荚膜多糖特异性单克隆抗体需要Fcγ受体III和巨噬细胞来介导小鼠抗肺炎球菌性肺炎的保护。

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Antibodies to pneumococcal capsular polysaccharide (PPS) are required for PPS-based vaccine-mediated protection against Streptococcus pneumoniae. Previous work established that 1E2, a mouse IgG1 to PPS3 that does not induce serotype 3 (ST3) S. pneumoniae killing by phagocytes in vitro, protects mice from death after intranasal infection with ST3, but its efficacy was abrogated in FcγR (F common gamma receptor)-deficient mice. In this study, we determined whether 1E2 efficacy against pulmonary ST3 infection requires FcγRIII. 1E2 did not protect FcγRIII-deficient (FcγRIII?/?) mice. Studies of the mechanism of 1E2-mediated effects showed that it resulted in a marked reduction in lung inflammation in ST3-infected wild-type (Wt [C57BL/6]) mice that was abrogated in FcγRIII?/? mice. 1E2 had no effect on early bacterial clearance in the lungs of ST3-infected Wt, FcγRIIB?/?, or FcγRIII?/? mice, but it reduced levels of bacteremia and serum macrophage inflammatory protein-2) (MIP-2), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α) in Wt and FcγRIIB?/? mice, strains in which it is protective. As previous work showed that neutrophils were dispensable for 1E2 efficacy, we investigated whether macrophages are required for 1E2 efficacy against intranasal infection with ST3 and found that its efficacy was abrogated in Wt mice depleted of macrophages intranasally. In vitro studies revealed that1E2 promoted ST3 internalization by na?ve alveolar macrophages but did not induce early intracellular killing. Macrophages from 1E2-treated ST3-infected mice studied ex vivo exhibited more apoptosis than those from FcγRIII?/? mice. These findings suggest that 1E2 mediates protection against ST3 in mice by affecting the inflammatory response, perhaps in part via macrophage apoptosis, rather than by inducing early bacterial clearance.
机译：基于PPS的疫苗介导的针对肺炎链球菌的保护需要抗肺炎球菌荚膜多糖（PPS）的抗体。先前的工作建立了1E2，它是小鼠IgG1至PPS3的抗体，它不会诱导体外吞噬细胞杀死血清型3（ST3）肺炎链球菌，可以保护小鼠免于经鼻内感染ST3后死亡。在FcγR（F常见伽玛受体）缺陷型小鼠中废除。在这项研究中，我们确定1E2对肺ST3感染的疗效是否需要FcγRIII。 1E2不能保护FcγRIII缺陷型（FcγRIII？/？）小鼠。对1E2介导的作用机理的研究表明，它导致ST3感染的野生型（Wt [C57BL / 6]）小鼠的肺部炎症显着减少，该小鼠在FcγRIII？/？老鼠。 1E2对ST3感染的Wt，FcγRIIB？/？或FcγRIII？/？小鼠的肺部早期细菌清除没有影响，但降低了细菌血症和Wt和FcγRIIB？/？小鼠中的血清巨噬细胞炎性蛋白2（MIP-2），白细胞介素6（IL-6）和肿瘤坏死因子α（TNF-α）这是保护性的。正如先前的研究表明，中性粒细胞对于1E2功效不可或缺，我们调查了巨噬细胞是否需要1E2才能抵抗鼻内ST3感染，并且发现其功效在鼻内耗竭巨噬细胞的Wt小鼠中被废除了。 体外研究表明，1E2可以促进幼稚的肺泡巨噬细胞促进ST3内在化，但不会引起早期的细胞内杀伤作用。体外研究[em> 的经1E2处理的经ST3感染的小鼠的巨噬细胞显示出比FcγRIIIα/β小鼠更大的凋亡。这些发现表明1E2可能通过影响炎症反应（可能部分是通过巨噬细胞凋亡而不是通过诱导早期细菌清除）来介导小鼠抗ST3的保护作用。

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