| First Author | Hung LY | Year | 2019 |
| Journal | Mucosal Immunol | Volume | 12 |
| Issue | 1 | Pages | 64-76 |
| PubMed ID | 30337651 | Mgi Jnum | J:279181 |
| Mgi Id | MGI:6356448 | Doi | 10.1038/s41385-018-0096-2 |
| Citation | Hung LY, et al. (2019) Macrophages promote epithelial proliferation following infectious and non-infectious lung injury through a Trefoil factor 2-dependent mechanism. Mucosal Immunol 12(1):64-76 |
| abstractText | Coordinated efforts between macrophages and epithelia are considered essential for wound healing, but the macrophage-derived molecules responsible for repair are poorly defined. This work demonstrates that lung macrophages rely upon Trefoil factor 2 to promote epithelial proliferation following damage caused by sterile wounding, Nippostrongylus brasiliensis or Bleomycin sulfate. Unexpectedly, the presence of T, B, or ILC populations was not essential for macrophage-driven repair. Instead, conditional deletion of TFF2 in myeloid-restricted CD11c(Cre) TFF2 (flox) mice exacerbated lung pathology and reduced the proliferative expansion of CD45(-) EpCAM(+) pro-SPC(+) alveolar type 2 cells. TFF2 deficient macrophages had reduced expression of the Wnt genes Wnt4 and Wnt16 and reconstitution of hookworm-infected CD11c(Cre) TFF2(flox) mice with rWnt4 and rWnt16 restored the proliferative defect in lung epithelia post-injury. These data reveal a previously unrecognized mechanism wherein lung myeloid phagocytes utilize a TFF2/Wnt axis as a mechanism that drives epithelial proliferation following lung injury. |
