Other
18 Authors
- Levine CB,
- Wang H,
- Cloutier N,
- Boor PJ,
- Ren P,
- Soong L,
- Shi PY,
- McLellan S,
- Sun J,
- Yang J,
- Zhang Y,
- Sun K,
- Hu H,
- Liang Y,
- Xie X,
- Gonzales C,
- Hosakote YM,
- Yu X
| First Author | Wang H | Year | 2024 |
| Journal | iScience | Volume | 27 |
| Issue | 6 | Pages | 110117 |
| PubMed ID | 38947521 | Mgi Jnum | J:351124 |
| Mgi Id | MGI:7663714 | Doi | 10.1016/j.isci.2024.110117 |
| Citation | Wang H, et al. (2024) The alarmin IL-33 exacerbates pulmonary inflammation and immune dysfunction in SARS-CoV-2 infection. iScience 27(6):110117 |
| abstractText | Dysregulated host immune responses contribute to disease severity and worsened prognosis in COVID-19 infection and the underlying mechanisms are not fully understood. In this study, we observed that IL-33, a damage-associated molecular pattern molecule, is significantly increased in COVID-19 patients and in SARS-CoV-2-infected mice. Using IL-33(-/-) mice, we demonstrated that IL-33 deficiency resulted in significant decreases in bodyweight loss, tissue viral burdens, and lung pathology. These improved outcomes in IL-33(-/-) mice also correlated with a reduction in innate immune cell infiltrates, i.e., neutrophils, macrophages, natural killer cells, and activated T cells in inflamed lungs. Lung RNA-seq results revealed that IL-33 signaling enhances activation of inflammatory pathways, including interferon signaling, pathogen phagocytosis, macrophage activation, and cytokine/chemokine signals. Overall, these findings demonstrate that the alarmin IL-33 plays a pathogenic role in SARS-CoV-2 infection and provides new insights that will inform the development of effective therapeutic strategies for COVID-19. |
