IL-17 is involved in Helicobacter pylori-induced gastric inflammatory responses in a mouse model.
IL-17 is involved in Helicobacter pylori-induced gastric inflammatory responses in a mouse model.
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DOI：
10.1111/j.1523-5378.2008.00629.x
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发表时间：
2008-12
期刊：
影响因子：
4.4
通讯作者：
Kita M
中科院分区：
文献类型：
--
作者：
Shiomi S;Toriie A;Imamura S;Konishi H;Mitsufuji S;Iwakura Y;Yamaoka Y;Ota H;Yamamoto T;Imanishi J;Kita M
幽门螺杆菌是慢性活动性胃炎和消化性溃疡的主要病因。最近的研究表明，幽门螺杆菌产生多种与中性粒细胞或单核细胞积累有关的细胞因子。白细胞介素-17 （IL-17）是一个新兴的炎性细胞因子家族的创始成员，其生物学活性尚未完全确定。本研究采用IL-17基因敲除（IL-17-/-）小鼠，研究IL-17在诱导胃炎症和保护幽门螺杆菌感染中的作用。用幽门螺杆菌CPY2052 （2 × 108 CFU/ml）攻毒IL-17-/和野生型C57BL/6小鼠，在规定时间进行组织学和微生物学评价。用ELISA试剂盒检测组织中IL-17和髓过氧化物酶（MPO）蛋白水平。在野生型小鼠中，IL-17在基线时未检测到，但在感染幽门螺杆菌后，IL-17的蛋白表达被诱导。野生型小鼠粘膜下层和固有层出现严重的中性粒细胞浸润。而IL-17-/-小鼠的中性粒细胞浸润程度明显低于野生型小鼠。虽然感染幽门螺杆菌的野生型小鼠的MPO活性明显高于未感染的野生型小鼠，但在感染IL-17-/-的小鼠中没有发现任何显著的酶活性增加。感染后1 ~ 6个月，IL-17-/-小鼠胃中幽门螺杆菌的定植数量明显低于野生型小鼠。这些结果提示IL-17可能在幽门螺杆菌感染的炎症反应中发挥重要作用，并最终影响幽门螺杆菌相关疾病的预后。
Helicobacter pylori (H. pylori) is the major cause of chronic active gastritis and peptic ulcer disease. Recent studies have shown that H. pylori produces various cytokines that are related to neutrophil or mononuclear cell accumulation. Interleukin-17 (IL-17) is the founding member of an emmerging family of inflammatory cytokines whose biological activities remain incompletely defined. In this study, the contributions of IL-17 to the induction of gastric inflammation and to the protection from H. pylori infection were investigated using IL-17 gene-knockout (IL-17-/-) mice. IL-17-/-and wild-type C57BL/6 mice were challenged with H. pylori CPY2052 (2 × 108 CFU/ml) and the histological and microbiological evaluation were carried out at specified times. IL-17 and myeloperoxidase (MPO) protein levels in tissues were assayed in duplicate using ELISA kits. In wild-type mice, IL-17 was undetected at baseline, however, the protein expression of IL-17 was induced after infection with H. pylori. A severe infiltration of neutrophils appeared in the submucosa and the lamina propria in wild-type mice. In contrast, the degree of neutrophil infiltration in IL-17-/- mice was significantly lower than that in wild-type mice. Although wild-type mice infected with H. pylori showed drastically higher MPO activity compared with uninfected wild-type mice, any significant increase in the enzyme activity was not revealed in infected IL-17-/- mice. The number of H. pylori colonized in the stomach of IL-17-/- mice was significantly lower than that of wild-type mice from 1 to 6 months after infection. These results suggest that IL-17 may play an important role in the inflammatory response to the H. pylori infection and ultimately influence the outcome of the H. pylori associated disease.
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影响因子：
14.2
作者：
Molet, S;Hamid, Q;Chakir, J
通讯作者：
Chakir, J
影响因子：
6.4
作者：
Huang, WT;Na, L;Schwarzenberger, P
通讯作者：
Schwarzenberger, P
影响因子：
4.3
作者：
Mizuno, Tomokazu;Ando, Takafumi;Goto, Hidemi
通讯作者：
Goto, Hidemi
影响因子：
3.1
作者：
Sebkova, L;Pellicanò, A;Luzza, F
通讯作者：
Luzza, F
影响因子：
4.8
作者：
Shalom-Barak, T;Quach, J;Lotz, M
通讯作者：
Lotz, M