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- W2897713835 abstract "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 CD11cCre 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 CD11cCre TFF2flox 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." @default.
- W2897713835 created "2018-10-26" @default.
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- W2897713835 date "2019-01-01" @default.
- W2897713835 modified "2023-10-13" @default.
- W2897713835 title "Macrophages promote epithelial proliferation following infectious and non-infectious lung injury through a Trefoil factor 2-dependent mechanism" @default.
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- W2897713835 doi "https://doi.org/10.1038/s41385-018-0096-2" @default.
- W2897713835 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6301101" @default.
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- W2897713835 hasPublicationYear "2019" @default.
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