The immunobiology of avian systemic salmonellosis
The immunobiology of avian systemic salmonellosis
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DOI：
10.1016/j.vetimm.2008.10.295
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发表时间：
2009-03-15
影响因子：
1.8
通讯作者：
Wigley, Paul
中科院分区：
文献类型：
--
作者：
Chappell, Lucy;Kaiser, Peter;Wigley, Paul
禽系统性沙门氏菌病主要由肠道沙门氏菌鸡血清型和鸡白痢血清型引起，分别引起鸡伤寒和鸡白痢。在感染期间，与免疫系统的相互作用发生在三个主要阶段。首先是通过胃肠道侵入。链球菌感染白痢或S.与S不同，鸡菌不会引起严重炎症。鼠伤寒沙门氏菌或S.肠道。通过体外模型发现S.鸡不诱导CXC趋化因子或促炎细胞因子如IL-1 β或IL-6的表达，而在体内模型S.鸡白痢感染导致回肠中CXCLi 1和CXCLi 2的下调。S. Gallinarum和S.鸡白痢意味着它们不被TLR 5识别，TLR 5被认为在炎症反应的启动中起关键作用，尽管其他病原体因子可能参与其中。第二阶段是建立全身感染。沙门氏菌侵入巨噬细胞和可能的树突状细胞，并转移到脾脏和肝脏，在那里发生复制。沙门氏菌的存活依赖于沙门氏菌致病岛2 III型分泌系统，其通过阻止溶菌酶与吞噬空泡的融合以及通过调节MHC和细胞因子表达来抑制抗微生物活性。在抗性和易感鸡品系中的研究表明，与巨噬细胞的相互作用是感染或免疫清除进展的核心。来自耐药动物的原代巨噬细胞通过呼吸爆发和诱导细胞因子表达（包括启动导致第三阶段的保护性Th 1应答）更有效地杀死沙门氏菌。如果沙门氏菌的复制不受控制，通常会导致动物死亡。如果先天免疫系统不能控制复制，那么主要通过Th 1相关细胞因子介导的细胞和体液应答能够清除感染。In S.鸡白痢有相当数量的动物发生脾巨噬细胞的持续感染。在这里，我们显示了初步的证据，适应性免疫的调制远离Th 1反应，以促进发展的载体状态。在携带者动物中，持续存在可能导致生殖道和鸡蛋感染，与母鸡性成熟开始相关的CD 4（+）T细胞数量和功能下降相关。(C)2008 Elsevier B. V.保留所有权利。
Avian systemic salmonellosis is primarily caused by Salmonella enterica serovar Gallinarum and serovar Pullorum causing the diseases Fowl Typhoid and Pullorum Disease respectively. During infection interaction with the immune system occurs in three main phases. First is invasion via the gastrointestinal tract. infection with S. Pullorum or S. Gallinarum does not cause substantial inflammation, unlike S. Typhimurium or S. Enteritidis. Through in vitro models it was found that S. Gallinarum does not induce expression of CXC chemokines or pro-inflammatory cytokines such as IL-1 P or IL-6, whilst in an in vivo model S. Pullorum infection leads to down-regulation of CXCLi1 and CXCLi2 in the ileum. The absence of flagella in S. Gallinarum and S. Pullorum means they are not recognised by TLR5, which is believed to play a key role in the initiation of inflammatory responses, though other pathogen-factors are likely to be involved. The second phase is establishing systemic infection. Salmonella invade macrophages and probably dendritic cells and are translocated to the spleen and liver, where replication occurs. Salmonella survival is dependent on the Salmonella pathogenicity island 2 type III secretion system, which inhibits antimicrobial activity by preventing fusion of lysosymes with the phagocytic vacuole and by modulation of MHC and cytokine expression. Studies in resistant and susceptible chicken lines have shown that the interaction with macrophages is central to the progression of infection or immunological clearance. Primary macrophages from resistant animals are more efficient in killing Salmonella through respiratory burst and by induction of cytokine expression including the initiation of protective Th1 responses that leads to the third phase. Where replication of Salmonella is not controlled the death of the animal usually results. If the innate immune system is not able to control replication then cellular and humoral responses, primarily mediated through Th1-associated cytokines, are able to clear infection. In S. Pullorum a significant number of animals develop persistent infection of splenic macrophages. Here we show preliminary evidence of modulation of adaptive immunity away from a Th1 response to facilitate the development of the carrier state. In carrier animals persistence may lead to reproductive tract and egg infection associated with a decline in CD4(+)T cell numbers and function associated with the onset of sexual maturity in hens. (C) 2008 Elsevier B.V. All rights reserved.