| First Author | Henkel M | Year | 2020 |
| Journal | Infect Immun | Volume | 89 |
| Issue | 1 | PubMed ID | 33077624 |
| Mgi Jnum | J:321871 | Mgi Id | MGI:6871776 |
| Doi | 10.1128/IAI.00298-20 | Citation | Henkel M, et al. (2020) Regulation of Pulmonary Bacterial Immunity by Follistatin-Like Protein 1. Infect Immun 89(1):e00298-20 |
| abstractText | Klebsiella pneumoniae is a common cause of antibiotic-resistant pneumonia. Follistatin-like protein 1 (FSTL-1) is highly expressed in the lung and is critical for lung homeostasis. The role of FSTL-1 in immunity to bacterial pneumonia is unknown. Wild-type (WT) and FSTL-1 hypomorphic (Hypo) mice were infected with Klebsiella pneumoniae to determine infectious burden, immune cell abundance, and cytokine production. FSTL-1 Hypo/TCRdelta(-/-) and FSTL-1 Hypo/IL17ra(-/-) were also generated to assess the role of gammadeltaT17 cells in this model. FSTL-1 Hypo mice had reduced K. pneumoniae lung burden compared with that of WT controls. FSTL-1 Hypo mice had increased Il17a/interleukin-17A (IL-17A) and IL-17-dependent cytokine expression. FSTL-1 Hypo lungs also had increased IL-17A(+) and TCRgammadelta(+) cells. FSTL-1 Hypo/TCRdelta(-/-) displayed a lung burden similar to that of FSTL-1 Hypo and reduced lung burden compared with the TCRdelta(-/-) controls. However, FSTL-1 Hypo/TCRdelta(-/-) mice had greater bacterial dissemination than FSTL-1 Hypo mice, suggesting that gamma delta T (gammadeltaT) cells are dispensable for FSTL-1 Hypo control of pulmonary infection but are required for dissemination control. Confusing these observations, FSTL-1 Hypo/TCRdelta(-/-) lungs had an increased percentage of IL-17A-producing cells compared with that of TCRdelta(-/-) mice. Removal of IL-17A signaling in the FSTL-1 Hypo mouse resulted in an increased lung burden. These findings identify a novel role for FSTL-1 in innate lung immunity to bacterial infection, suggesting that FSTL-1 influences type-17 pulmonary bacterial immunity. |
