THE ROLE OF SPECIFIC IgG AND COMPLEMENT IN COMBATING A PRIMARY MUCOSAL INFECTION OF THE GUT EPITHELIUM

THE ROLE OF SPECIFIC IgG AND COMPLEMENT IN COMBATING A PRIMARY MUCOSAL INFECTION OF THE GUT EPITHELIUM
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DOI:
10.1556/eujmi.1.2011.4.7
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发表时间:
2011-12-01
影响因子:
2.2
通讯作者:
Bry, L.
Bry, L.
中科院分区:
其他
文献类型:
--
作者:
Belzer, C.;Liu, Q.;Bry, L.

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补体和补体固定IgG同种型在粘膜表面的作用不明确。先前的数据已经证明,感染附着和消退病原体啮齿类柠檬酸杆菌的存活需要产生全身性和CD4(+)T细胞依赖性IgG。我们已经发现,补体和补体固定IgG同种型都是C.啮齿类感染我们的研究结果表明,IgG和补体C3b进入肠腔,并结合上皮粘附,粪便脱落的C。啮齿动物。此外,C3缺陷型小鼠表现出严重的存活缺陷,尽管在全身或粘膜部位补充C3的方法恢复了宿主中补体的保护能力。我们的数据提供的证据表明,IgG和补体建设性地相互作用的上皮细胞的两侧,以打击殖民粘膜感染。
The role of complement and complement-fixing IgG isotypes at mucosal surfaces is ill defined. Previous data have demonstrated that survival of an infection with the attaching and effacing pathogen Citrobacter rodentium requires production of systemic and CD4(+) T cell-dependent IgG. We have found that both complement and complement-fixing IgG isotypes are needed to survive a C. rodentium infection. Our results indicate that both IgG and complement C3b enter the gut lumen and bind epithelially adherent, and fecally shed C. rodentium. Furthermore, C3-deficient mice demonstrate a profound survival defect, though means to replenish C3 in systemic or mucosal sites restores the protective capacity of complement in the host. Our data provide evidence that both IgG and complement interact constructively on both sides of the epithelium to fight colonizing mucosal infections.