Evidence for interleukin-1-independent stimulation of interleukin-12 and down-regulation by interleukin-10 in Helicobacter pylori-infected murine dendritic cells deficient in the interleukin-1 receptor.
Evidence for interleukin-1-independent stimulation of interleukin-12 and down-regulation by interleukin-10 in Helicobacter pylori-infected murine dendritic cells deficient in the interleukin-1 receptor.
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在幽门螺杆菌感染且缺乏白细胞介素 1 受体的鼠树突状细胞中，白细胞介素 12 受到白细胞介素 12 的独立刺激和白细胞介素 10 的下调的证据。
DOI：
10.1111/j.1574-695x.2006.00105.x
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Guiney,DonaldG
中科院分区：
文献类型：
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作者：
Obonyo,Marygorret;Cole,SheriP;Datta,SandipK;Guiney,DonaldG
幽门螺杆菌感染的特征是免疫系统细胞，包括树突状细胞，浸润到胃粘膜中。在幽门螺杆菌感染的慢性炎症过程中，多种细胞因子被分泌到粘膜中，包括白细胞介素-1 β（IL-1β）。IL-1在H.使用来自野生型和IL-1受体缺陷（IL-1 R −/−）小鼠的骨髓来源的树突状细胞研究幽门螺杆菌感染。树突状细胞与H.幽门螺杆菌感染复数为10和100，并评估细胞因子的产生。pyloriSD 4和SD 4的同基因cagE突变体在来自野生型和IL-1 R −/−小鼠的树突状细胞中以相当的水平刺激IL-12、IL-6、IL-1β、IL-10和肿瘤坏死因子-α。IL-10的产生需要较高的接种量，而IL-12在该细菌负荷下降低。用IL-10的抗体预处理树突状细胞导致IL-12的产生增加，证实了IL-10对IL-12的下调。幽门。我们推测，在较高的感染复数下，IL-10下调IL-12代表了vivobyH对宿主炎症反应的调节。当细菌负荷很高时，幽门螺杆菌会被感染，从而允许胃粘膜的持续定植。
Helicobacter pyloriinfection is characterized by infiltration of cells of the immune system, including dendritic cells, into the gastric mucosa. During chronic inflammation withHelicobacter pyloriinfection, a variety of cytokines are secreted into the mucosa, including interleukin-1β (IL-1β). The role of IL-1 inH. pyloriinfection was investigated using bone-marrow-derived dendritic cells from wild-type and IL-1 receptor-deficient (IL-1R−/−) mice. Dendritic cells were incubated withH. pyloriat a multiplicity of infection of 10 and 100, and cytokine production evaluated.Helicobacter pyloriSS1,H. pyloriSD4, and an isogeniccagE mutant of SD4 stimulated IL-12, IL-6, IL-1β, IL-10, and tumor necrosis factor-alpha at comparable levels in dendritic cells from both wild-type and IL-1R−/−mice. IL-10 production required the higher inoculum, while IL-12 was decreased at this bacterial load. Pretreatment of dendritic cells with an antibody to IL-10 resulted in an increased production of IL-12, confirming the down-regulation of IL-12 by IL-10.cagE was required for maximum stimulation of IL-12 byH. pylori. We speculate that the down-regulation of IL-12 by IL-10 at the higher multiplicity of infection represents the modulation of the host inflammatory responsein vivobyH. pyloriwhen the bacterial load is high, allowing for persistent colonization of the gastric mucosa.