Other
14 Authors
- Williams J,
- Myerburg MM,
- Das S,
- Chen J,
- Kolls JK,
- Hu S,
- Ray P,
- Wenzel SE,
- Zhao J,
- St Croix C,
- Pilewski JM,
- Good M,
- Ross M,
- Ray A
| First Author | Das S | Year | 2020 |
| Journal | iScience | Volume | 23 |
| Issue | 7 | Pages | 101256 |
| PubMed ID | 32580124 | Mgi Jnum | J:350017 |
| Mgi Id | MGI:6717602 | Doi | 10.1016/j.isci.2020.101256 |
| Citation | Das S, et al. (2020) Interleukin-22 Inhibits Respiratory Syncytial Virus Production by Blocking Virus-Mediated Subversion of Cellular Autophagy. iScience 23(7):101256 |
| abstractText | Respiratory syncytial virus (RSV) infection can cause severe bronchiolitis in infants requiring hospitalization, whereas the elderly and immunocompromised are prone to RSV-induced pneumonia. RSV primarily infects lung epithelial cells. Given that no vaccine against RSV is currently available, we tested the ability of the epithelial-barrier protective cytokine interleukin-22 (IL-22) to control RSV production. When used in a therapeutic modality, IL-22 efficiently blunted RSV production from infected human airway and alveolar epithelial cells and IL-22 administration drastically reduced virus titer in the lungs of infected newborn mice. RSV infection resulted in increased expression of LC3B, a key component of the cellular autophagic machinery, and knockdown of LC3B ablated virus production. RSV subverted LC3B with evidence of co-localization and caused a significant reduction in autophagic flux, both reversed by IL-22 treatment. Our findings inform a previously unrecognized anti-viral effect of IL-22 that can be harnessed to prevent RSV-induced severe respiratory disease. |
