IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse model
The immune response to Helicobacter pylori 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 contr...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2012-03-01
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| Series: | Frontiers in Immunology |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fimmu.2012.00056/full |
| _version_ | 1828352933980274688 |
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| author | Dennis J Horvath Mary Kay Washington Vicki A Cope Holly Marie Scott Algood Holly Marie Scott Algood |
| author_facet | Dennis J Horvath Mary Kay Washington Vicki A Cope Holly Marie Scott Algood Holly Marie Scott Algood |
| author_sort | Dennis J Horvath |
| collection | DOAJ |
| description | The immune response to Helicobacter pylori 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. pylori colonization in the stomach. The relative contributions of these subsets to gastritis and control of infection are still under investigation. Expression of IL-23, which is induced in dendritic cells and macrophages following co-culture with H. pylori, has also been reported to increase during H. pylori infection in humans and animal models. IL-23 plays a role in stabilizing and expanding Th-17 cell cytokine expression. To investigate the role of IL-23 in H. pylori, we infected IL-23 deficient mice and wild-type littermates with H. pylori strain SS1. At various time points post-infection, we assessed colonization, gastric inflammation, and cytokine profiles in the gastric tissue. Specifically, H. pylori-infected IL-23-/- mice have higher levels of H. pylori 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. pylori infected IL-23-/- had mild increases in our measurements of disease severity. Our results indicate that IL-23 plays a minor role in the activation of the immune response and induction of gastritis in response to H. pylori by contributing to the control of infection and severity of gastritis. |
| first_indexed | 2024-04-14T02:00:20Z |
| format | Article |
| id | doaj.art-a2c17d4b402c4d1292b9ef30a8ccb98d |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-04-14T02:00:20Z |
| publishDate | 2012-03-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-a2c17d4b402c4d1292b9ef30a8ccb98d2022-12-22T02:18:50ZengFrontiers Media S.A.Frontiers in Immunology1664-32242012-03-01310.3389/fimmu.2012.0005620684IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse modelDennis J Horvath0Mary Kay Washington1Vicki A Cope2Holly Marie Scott Algood3Holly Marie Scott Algood4Vanderbilt UniversityVanderbilt University School of MedicineVanderbilt UniversityDepartment of Veteran's AffairsVanderbilt UniversityThe immune response to Helicobacter pylori 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. pylori colonization in the stomach. The relative contributions of these subsets to gastritis and control of infection are still under investigation. Expression of IL-23, which is induced in dendritic cells and macrophages following co-culture with H. pylori, has also been reported to increase during H. pylori infection in humans and animal models. IL-23 plays a role in stabilizing and expanding Th-17 cell cytokine expression. To investigate the role of IL-23 in H. pylori, we infected IL-23 deficient mice and wild-type littermates with H. pylori strain SS1. At various time points post-infection, we assessed colonization, gastric inflammation, and cytokine profiles in the gastric tissue. Specifically, H. pylori-infected IL-23-/- mice have higher levels of H. pylori 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. pylori infected IL-23-/- had mild increases in our measurements of disease severity. Our results indicate that IL-23 plays a minor role in the activation of the immune response and induction of gastritis in response to H. pylori by contributing to the control of infection and severity of gastritis.http://journal.frontiersin.org/Journal/10.3389/fimmu.2012.00056/fullCytokinesGastritisHelicobacter pyloriT lymphocytesInterleukin 17interleukin 23 |
| spellingShingle | Dennis J Horvath Mary Kay Washington Vicki A Cope Holly Marie Scott Algood Holly Marie Scott Algood IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse model Frontiers in Immunology Cytokines Gastritis Helicobacter pylori T lymphocytes Interleukin 17 interleukin 23 |
| title | IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse model |
| title_full | IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse model |
| title_fullStr | IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse model |
| title_full_unstemmed | IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse model |
| title_short | IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse model |
| title_sort | il 23 contributes to control of chronic helicobacter pylori infection and the development of t helper responses in a mouse model |
| topic | Cytokines Gastritis Helicobacter pylori T lymphocytes Interleukin 17 interleukin 23 |
| url | http://journal.frontiersin.org/Journal/10.3389/fimmu.2012.00056/full |
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