Group 2 Innate Lymphoid Cells Protect Mice from Abdominal Aortic Aneurysm Formation via IL5 and Eosinophils
Abstract Development of abdominal aortic aneurysms (AAA) enhances lesion group‐2 innate lymphoid cell (ILC2) accumulation and blood IL5. ILC2 deficiency in Rorafl/flIl7rCre/+ mice or induced ILC2 depletion in Icosfl‐DTR‐fl/+Cd4Cre/+ mice expedites AAA growth, increases lesion inflammation, but leads...
| Main Authors: | , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2023-03-01
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| Series: | Advanced Science |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/advs.202206958 |
| _version_ | 1811160431520120832 |
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| author | Yuanyuan Zhang Tianxiao Liu Zhiyong Deng Wenqian Fang Xian Zhang Shuya Zhang Minjie Wang Songyuan Luo Zhaojie Meng Jing Liu Galina K. Sukhova Dazhu Li Andrew N. J. McKenzie Peter Libby Guo‐Ping Shi Junli Guo |
| author_facet | Yuanyuan Zhang Tianxiao Liu Zhiyong Deng Wenqian Fang Xian Zhang Shuya Zhang Minjie Wang Songyuan Luo Zhaojie Meng Jing Liu Galina K. Sukhova Dazhu Li Andrew N. J. McKenzie Peter Libby Guo‐Ping Shi Junli Guo |
| author_sort | Yuanyuan Zhang |
| collection | DOAJ |
| description | Abstract Development of abdominal aortic aneurysms (AAA) enhances lesion group‐2 innate lymphoid cell (ILC2) accumulation and blood IL5. ILC2 deficiency in Rorafl/flIl7rCre/+ mice or induced ILC2 depletion in Icosfl‐DTR‐fl/+Cd4Cre/+ mice expedites AAA growth, increases lesion inflammation, but leads to systemic IL5 and eosinophil (EOS) deficiency. Mechanistic studies show that ILC2 protect mice from AAA formation via IL5 and EOS. IL5 or ILC2 from wild‐type (WT) mice, but not ILC2 from Il5−/− mice induces EOS differentiation in bone‐marrow cells from Rorafl/flIl7rCre/+ mice. IL5, IL13, and EOS or ILC2 from WT mice, but not ILC2 from Il5−/− and Il13−/− mice block SMC apoptosis and promote SMC proliferation. EOS but not ILC2 from WT or Il5−/− mice block endothelial cell (EC) adhesion molecule expression, angiogenesis, dendritic cell differentiation, and Ly6Chi monocyte polarization. Reconstitution of WT EOS and ILC2 but not Il5−/− ILC2 slows AAA growth in Rorafl/flIl7rCre/+ mice by increasing systemic EOS. Besides regulating SMC pathobiology, ILC2 play an indirect role in AAA protection via the IL5 and EOS mechanism. |
| first_indexed | 2024-04-10T05:57:11Z |
| format | Article |
| id | doaj.art-5088f16849cc46d4b5b3ce3f82354472 |
| institution | Directory Open Access Journal |
| issn | 2198-3844 |
| language | English |
| last_indexed | 2024-04-10T05:57:11Z |
| publishDate | 2023-03-01 |
| publisher | Wiley |
| record_format | Article |
| series | Advanced Science |
| spelling | doaj.art-5088f16849cc46d4b5b3ce3f823544722023-03-03T08:59:14ZengWileyAdvanced Science2198-38442023-03-01107n/an/a10.1002/advs.202206958Group 2 Innate Lymphoid Cells Protect Mice from Abdominal Aortic Aneurysm Formation via IL5 and EosinophilsYuanyuan Zhang0Tianxiao Liu1Zhiyong Deng2Wenqian Fang3Xian Zhang4Shuya Zhang5Minjie Wang6Songyuan Luo7Zhaojie Meng8Jing Liu9Galina K. Sukhova10Dazhu Li11Andrew N. J. McKenzie12Peter Libby13Guo‐Ping Shi14Junli Guo15Hainan Provincial Key Laboratory for Tropical Cardiovascular Diseases Research, Key Laboratory of Emergency and Trauma of Ministry of Education Institute of Cardiovascular Research of the First Affiliated HospitalHainan Medical University Haikou 571199 ChinaDepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USADepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USADepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USADepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USAHainan Provincial Key Laboratory for Tropical Cardiovascular Diseases Research, Key Laboratory of Emergency and Trauma of Ministry of Education Institute of Cardiovascular Research of the First Affiliated HospitalHainan Medical University Haikou 571199 ChinaDepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USADepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USADepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USADepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USADepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USADepartment of Cardiology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 ChinaDivision of Protein & Nucleic Acid Chemistry MRC Laboratory of Molecular Biology Cambridge CB2 0QH UKDepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USADepartment of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA 02115 USAHainan Provincial Key Laboratory for Tropical Cardiovascular Diseases Research, Key Laboratory of Emergency and Trauma of Ministry of Education Institute of Cardiovascular Research of the First Affiliated HospitalHainan Medical University Haikou 571199 ChinaAbstract Development of abdominal aortic aneurysms (AAA) enhances lesion group‐2 innate lymphoid cell (ILC2) accumulation and blood IL5. ILC2 deficiency in Rorafl/flIl7rCre/+ mice or induced ILC2 depletion in Icosfl‐DTR‐fl/+Cd4Cre/+ mice expedites AAA growth, increases lesion inflammation, but leads to systemic IL5 and eosinophil (EOS) deficiency. Mechanistic studies show that ILC2 protect mice from AAA formation via IL5 and EOS. IL5 or ILC2 from wild‐type (WT) mice, but not ILC2 from Il5−/− mice induces EOS differentiation in bone‐marrow cells from Rorafl/flIl7rCre/+ mice. IL5, IL13, and EOS or ILC2 from WT mice, but not ILC2 from Il5−/− and Il13−/− mice block SMC apoptosis and promote SMC proliferation. EOS but not ILC2 from WT or Il5−/− mice block endothelial cell (EC) adhesion molecule expression, angiogenesis, dendritic cell differentiation, and Ly6Chi monocyte polarization. Reconstitution of WT EOS and ILC2 but not Il5−/− ILC2 slows AAA growth in Rorafl/flIl7rCre/+ mice by increasing systemic EOS. Besides regulating SMC pathobiology, ILC2 play an indirect role in AAA protection via the IL5 and EOS mechanism.https://doi.org/10.1002/advs.202206958abdominal aortic aneurysmeosinophilGroup‐2 innate lymphoid cellIL5 |
| spellingShingle | Yuanyuan Zhang Tianxiao Liu Zhiyong Deng Wenqian Fang Xian Zhang Shuya Zhang Minjie Wang Songyuan Luo Zhaojie Meng Jing Liu Galina K. Sukhova Dazhu Li Andrew N. J. McKenzie Peter Libby Guo‐Ping Shi Junli Guo Group 2 Innate Lymphoid Cells Protect Mice from Abdominal Aortic Aneurysm Formation via IL5 and Eosinophils Advanced Science abdominal aortic aneurysm eosinophil Group‐2 innate lymphoid cell IL5 |
| title | Group 2 Innate Lymphoid Cells Protect Mice from Abdominal Aortic Aneurysm Formation via IL5 and Eosinophils |
| title_full | Group 2 Innate Lymphoid Cells Protect Mice from Abdominal Aortic Aneurysm Formation via IL5 and Eosinophils |
| title_fullStr | Group 2 Innate Lymphoid Cells Protect Mice from Abdominal Aortic Aneurysm Formation via IL5 and Eosinophils |
| title_full_unstemmed | Group 2 Innate Lymphoid Cells Protect Mice from Abdominal Aortic Aneurysm Formation via IL5 and Eosinophils |
| title_short | Group 2 Innate Lymphoid Cells Protect Mice from Abdominal Aortic Aneurysm Formation via IL5 and Eosinophils |
| title_sort | group 2 innate lymphoid cells protect mice from abdominal aortic aneurysm formation via il5 and eosinophils |
| topic | abdominal aortic aneurysm eosinophil Group‐2 innate lymphoid cell IL5 |
| url | https://doi.org/10.1002/advs.202206958 |
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