Helicobacter pylori-Induced Th17 Responses Modulate Th1 Cell Responses, Benefit Bacterial Growth, and Contribute to Pathology in Mice
| Autor: | Hong Guo, Wei Ying Zhou, Richard A. Flavell, Yuan Zhuang, Bin Xiao, Ke Ran Jia, Feng Jun Wang, Gang Guo, Wei Jun Zhang, Tao Liu, Kai Yun Liu, Yun Shi, Chao Wu, Quan Ming Zou, Xiao Fei Liu, Zhinan Yin, Zhuo Zhao, Jin Yu Zhang, Ying Guo, Xu Hu Mao |
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| Rok vydání: | 2010 |
| Předmět: |
Pathology
medicine.medical_specialty T cell Immunology Cell Down-Regulation Inflammation Bacterial growth Interleukin-23 Helicobacter Infections law.invention Pathogenesis Interferon-gamma Mice T-Lymphocyte Subsets law medicine Animals Immunology and Allergy Mice Knockout Mice Inbred BALB C Helicobacter pylori biology Stomach Interleukin-17 Th1 Cells bacterial infections and mycoses biology.organism_classification Interleukin-12 Up-Regulation Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure Recombinant DNA Female medicine.symptom Signal Transduction |
| Zdroj: | The Journal of Immunology. 184:5121-5129 |
| ISSN: | 1550-6606 0022-1767 |
| Popis: | CD4+ T cell responses are critical for the pathogenesis of Helicobacter pylori infection. The present study evaluated the role of the Th17 subset in H. pylori infection. H. pylori infection induced significant expression of IL-17 and IFN-γ in mouse gastric tissue. IL-23 and IL-12 were increased in the gastric tissue and in H. pylori-stimulated macrophages. Cell responses were examined by intracellular staining for IFN-γ, IL-4, and IL-17. Mice infected with H. pylori developed a mixed Th17/Th1 response; Th17 responses preceded Th1 responses. Treatment of mice with an anti–IL-17 Ab but not a control Ab significantly reduced the H. pylori burden and inflammation in the stomach. H. pylori colonization and gastric inflammation were also lower in IL-17−/− mice. Furthermore, administration of recombinant adenovirus encoding mouse IL-17 increased both H. pylori load and inflammation. Further analysis showed that the Th1 cell responses to H. pylori were downregulated when IL-17 is deficient. These results together suggest that H. pylori infection induces a mixed Th17/Th1 cell response and the Th17/IL-17 pathway modulates Th1 cell responses and contributes to pathology. |
| Databáze: | OpenAIRE |
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