IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse model
IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse model
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DOI：
10.3389/fimmu.2012.00056
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发表时间：
2012-01-01
影响因子：
7.3
通讯作者：
Algood, Holly M. Scott
中科院分区：
文献类型：
--
作者：
Horvath, Dennis J., Jr.;Washington, M. Kay;Algood, Holly M. Scott
幽门螺杆菌的免疫应答包括T辅助细胞-1、T辅助细胞2和T辅助细胞17的混合应答。已有研究表明，在感染过程中，辅助性T细胞参与了胃炎性反应，而辅助性T细胞1(Th1)和辅助性T细胞17(Th17)亚群可能是控制幽门螺杆菌在胃内定植所必需的。这些亚群对胃炎和感染控制的相对贡献仍在调查中。LI-23具有稳定和扩增Th17细胞因子表达的作用。与幽门螺杆菌共培养后，在树突状细胞和巨噬细胞中诱导的IL-23的表达也被报道在人和动物模型感染幽门螺杆菌的过程中增加。为了研究IL-23在幽门螺杆菌中的作用，我们用幽门螺杆菌SS1株感染IL-23p19缺陷小鼠(IL-23-/-)和野生型窝产仔。在感染后的不同时间点，我们评估了定植、胃炎症和胃组织中的细胞因子谱。具体地说，与幽门螺杆菌感染的野生型小鼠相比，幽门螺杆菌感染的IL23-/-小鼠的胃中幽门螺杆菌水平更高，慢性胃炎显著减少，IL-17和干扰素γ的表达减少。虽然这些差异中的许多是显著的，但感染了IL-23-/-的幽门螺杆菌在我们的疾病严重程度测量中有轻微的增加。我们的结果表明，IL-23通过控制感染和胃炎的严重程度，在激活免疫反应和诱导幽门螺杆菌引起的胃炎中发挥作用。
The immune response to Helicobacter pylon involves a mixed T helper-1, T helper-2, and T helper-17 response. It has been suggested that T helper cells contribute to the gastric inflammatory response during infection, and that T helper 1 (Th1) and T helper 17 (Th17) subsets may be required for control of H. pylon colonization in the stomach. The relative contributions of these subsets to gastritis and control of infection are still under investigation. LI-23 plays a role in stabilizing and expanding Th17 cell cytokine expression. Expression of IL-23, which is induced in dendritic cells and macrophages following co-culture with H. pylon, has also been reported to increase during H. pylon infection in humans and animal models. To investigate the role of IL-23 in H. pylon, we infected IL-23p19 deficient mice (IL-23-/-) and wild-type littermates with H. pylon strain SS1. At various time points post-infection, we assessed colonization, gastric inflammation, and cytokine profiles in the gastric tissue. Specifically, H. pylori-infected IL23-/- mice have higher levels of H. pylon in their stomachs, significantly less chronic gastritis, and reduced expression of IL-17 and IFN gamma compared to H. pylori-infected wild-type mice. While many of these differences were significant, the H. pylon infected IL-23-/- had mild increases in our measurements of disease severity. Our results indicate that IL-23 plays a role in the activation of the immune response and induction of gastritis in response to H. pylon by contributing to the control of infection and severity of gastritis.