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Publication Detail

Title: Macrophages promote epithelial proliferation following infectious and non-infectious lung injury through a Trefoil factor 2-dependent mechanism.

Authors: Hung, Li-Yin; Sen, Debasish; Oniskey, Taylor K; Katzen, Jeremey; Cohen, Noam A; Vaughan, Andrew E; Nieves, Wildaliz; Urisman, Anatoly; Beers, Michael F; Krummel, Matthew F; Herbert, De'Broski R

Published In Mucosal Immunol, (2019 Jan)

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.

PubMed ID: 30337651 Exiting the NIEHS site

MeSH Terms: Animals; Bleomycin; CD11c Antigen/metabolism; Cell Communication; Cell Proliferation; Cells, Cultured; Humans; Lung Injury/chemically induced; Lung Injury/immunology*; Lung Injury/parasitology; Lung/immunology*; Lung/pathology; Macrophages/physiology*; Mice; Mice, Inbred C57BL; Mice, Knockout; Nippostrongylus/immunology*; Respiratory Mucosa/physiology*; Strongylida Infections/immunology*; Trefoil Factor-2/genetics; Trefoil Factor-2/metabolism*; Wound Healing

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