期刊
MUCOSAL IMMUNOLOGY
卷 12, 期 1, 页码 64-76出版社
SPRINGERNATURE
DOI: 10.1038/s41385-018-0096-2
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类别
资金
- NIH [AI095289, GM083204, UO1AI125940]
- Burroughs Wellcome Fund
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(vertical bar) pro-SPC vertical bar 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.
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