The in vivo T helper type 17 and regulatory T cell immune responses to Aggregatibacter actinomycetemcomitans.
The in vivo T helper type 17 and regulatory T cell immune responses to Aggregatibacter actinomycetemcomitans.
复制标题
体内 T 辅助细胞 17 型和调节性 T 细胞对放线菌聚集菌的免疫反应。
DOI：
10.1111/omi.12187
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发表时间：
2017
影响因子：
3.7
通讯作者：
Sedghizadeh,PP
中科院分区：
文献类型：
--
作者：
Mahabady,S;Tjokro,N;Aharonian,S;Zadeh,HH;Chen,C;Allayee,H;Sedghizadeh,PP
已知牙周病原体放线菌聚集菌可在感染宿主中引发全身免疫反应，偶尔会引起非口腔感染。关于其免疫病理学反应和细菌毒力因子参与的详细信息仍有待阐明。本研究的目的是评估对 A 的全身免疫反应。 放线菌伴随口腔感染。我们使用动物模型，通过注射活野生型（WT）D7S-1和白细胞毒素和细胞致死膨胀毒素（ΔltxΔcdt）A的双敲除突变体来模拟细菌的全身传播。 大鼠口腔粘膜中的伴放线菌菌株。检查引流淋巴结中的调节性 T (Treg) 和 17 型辅助性 T (Th17) 细胞亚群及其相关介质。在 3 周的实验期间，用 WT 和 ΔltxΔcdt 攻击的大鼠也观察到 Th17 细胞比例的增加和 Treg 细胞的减少。注意到 Th17 基因通路中促炎细胞因子的显着上调和下调，以及 WT 和 ΔltxΔcdt 之间的一些定性差异。此外，我们观察到与 D7S-1 组相比，接种 ΔltxΔcdt 的大鼠中与促炎反应相关的关键基因的折叠调节存在差异。这表明，虽然这两个毒力因子（ΔltxΔcdt）的敲除可能会抑制某些促炎基因，但与D7S-1相比，它会导致其他基因类似的过度表达，表明A的致病性中仍然存在一个共同因素。 伴放线菌。
The periodontal pathogenAggregatibacter actinomycetemcomitansis known to elicit a systemic immune response in the infected host, and occasionally causes non‐oral infections. Detailed information on its immunopathological responses and the involvement of bacterial virulence factors remains to be elucidated. The aim of this study was to assess the systemic immune response toA. actinomycetemcomitansoral infection. We used an animal model that simulates systemic dissemination of the bacteria by injecting live wild‐type (WT) D7S‐1 and a double knockout mutant of leukotoxin and cytolethal distending toxin (ΔltxΔcdt)A. actinomycetemcomitansstrains in rat oral mucosa. Draining lymph nodes were examined for regulatory T (Treg) and T helper type 17 (Th17) cell subsets and their associated mediators. An increase in the proportion of Th17 cells and a decrease in Treg cells over the experimental period of 3 weeks were similarly observed for rats challenged with WT and ΔltxΔcdt. Significant upregulation and downregulation of proinflammatory cytokines in the Th17 gene pathway was noted, as well as several qualitative differences between WT and ΔltxΔcdt. Furthermore, we observed differential fold regulation in key genes associated with a proinflammatory response inΔltxΔcdt‐inoculated rats relative to D7S‐1 group. This suggests that although the knockout of these two virulence factors (ΔltxΔcdt) may suppress certain proinflammatory genes, it causes similar over‐expression of other genes compared with D7S‐1, indicating a common factor that still remains in the pathogenicity ofA. actinomycetemcomitans.