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

Hung LY
University of Pennsylvania
October 9, 2018
Mucosal Immunol
https://pubmed.ncbi.nlm.nih.gov/30337651

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/30337651

Research summary

Lung macrophages require TFF2 to drive alveolar type 2‑cell proliferation after sterile injury, helminth infection (Nippostrongylus brasiliensis), or bleomycin exposure. Conditional deletion of Tff2 in myeloid cells (CD11c^Cre Tff2^flox) impaired repair, reduced macrophage Wnt4/Wnt16 expression, and worsened pathology; recombinant Wnt4/Wnt16 rescued proliferation.

Key outcome of the study

Myeloid Tff2 supports AT2 proliferation via Wnt4/Wnt16; loss of Tff2 impairs lung repair; recombinant Wnts restore regeneration

Model

CD11c^Cre; Tff2^flox myeloid‑specific conditional KO mouse — genOway-developed (C57BL/6 background)

TARGET:
Tff2
Synonyms:
mSP; SP; Sml1; Spasmolytic polypeptide; Spasmolytic protein 1

Keywords

Lung tissue repair; epithelial regeneration; macrophage–epithelium crosstalk; Wnt signaling; helminth infection; sterile injury

Technical specifications

Conditional knockout; Cre‑loxP (CD11c); lung injury models (bleomycin, helminth); recombinant ligand rescue

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