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首页> 外文期刊>Infection and immunity >Role of host factors in the pathogenesis of Salmonella-associated arthritis in rats.
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Role of host factors in the pathogenesis of Salmonella-associated arthritis in rats.

机译：宿主因子在大鼠沙门氏菌相关关节炎的发病机制中的作用。

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摘要

To evaluate the roles of the infectious agent and the host in the pathogensis of Salmonella-associated arthritis (SAA), 1O(3) to 10(6) heat-killed Salmonella enteritidis were injected directly into involved carpal joints in normal and actively immunized rats and in hosts adoptively immunized by the intravenous transfer of spleen cells from syngeneic donors with ongoing SAA. As many as 10(6) living Salmonellae invariably failed to generate more than a transient inflammatory response in normal rats. The regression of acute joint swelling was accelerated in both types of immunized hosts. The intensity and duration of acute inflammation evoked in normal rats by 10(6) and 10(9) heat-killed Salmonellae did not exceed the response elicited by 10(3) living organisms. In sharply contrasting results, however, a chronic arthritis became established in a significant number of actively and adoptively sensitized rats after the intra-articular injection of 10(9) heat-killed organisms. No Salmonellae were recovered from these adoptively sensitized rats although small numbers of organisms has been present among the spleen cells in the transfer inocula. Taken together, these results indicate the obligatory involvement of host factors in the mediation of this chronic arthritis and virtually eliminate any likelihood that joint damage in SAA is due to the directly destructive effects of intra-articular infection.
机译：为了评估感染剂和宿主在沙门氏菌相关关节炎（SAA）病原学中的作用，将1O（3）至10（6）热杀死的肠炎沙门氏菌直接注射到正常和主动免疫大鼠的腕关节中并通过持续性SAA静脉注射来自同系供体的脾细胞来过继免疫。在正常大鼠中，多达10（6）个活的沙门氏菌始终未能产生更多的瞬时炎症反应。两种类型的免疫宿主均加速了急性关节肿胀的消退。 10（6）和10（9）热杀死的沙门氏菌在正常大鼠中诱发的急性炎症的强度和持续时间不超过10（3）个活生物体引起的反应。然而，与之形成鲜明对比的结果是，在关节内注射10（9）个热灭活的生物后，在大量活跃和过继致敏的大鼠中建立了慢性关节炎。从这些过继敏化的大鼠中未回收沙门氏菌，尽管在转移接种物中的脾细胞中存在少量生物。综上所述，这些结果表明宿主因素必须参与这种慢性关节炎的介导，并且实际上消除了SAA关节损伤是由于关节内感染的直接破坏作用而引起的任何可能性。

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