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

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

New Insights from Seafloor Mapping of a Hawaiian Marine Monument

On 15 June 2006, when U.S. President George W. Bush signed the proclamation creating the Papahānaumokuākea Marine National Monument (PMNM), he probably wasn’t thinking about underwater morphology. To fully understand the coral reefs and marine ecosystems that the monument was created to protect, however, scientists need to have a detailed picture of the seafloor features, home to corals and other species, as well as the geologic history of the area. Thanks to a recent, multi-institution expedition, such a seafloor features that will not only inform conservation efforts but also enable geologists and geophysicists to revise their understanding of Hawaii’s complex geologic past. Specifically, data should help scientists answer fundamental questions about the area’s regional geology. For instance, which seamounts were truly formed because of Hawaiian hotspot volcanism, and which seamounts were not

Raw GGP HD150K SNP data for 9 Russian cattle breeds

This set includes 9 Russian cattle breeds genotyped on the GeneSeek HD150K SNP array. The breeds included are: Kalmyk, Buryat, Yakut, Kazakh Whiteheaded, Kostroma, Kholmogory, Bestuzhev, Yaroslavl, and Black Pied

GGP HD150K SNP data for 10 breeds of European origin

This set includes autosomal genotyping data for 6 Russian breeds of European origin genotyped on the GeneSeeek HD150K SNP array (MAF<0.05): Bestuzhev, Black Pied, Kazakh Whiteheaded, Kholmogory, Kostroma, and Yaroslavl combined with sequence-based genotypes of Angus, Holstein, Jersey, and Fleckvieh from the 1000 bull genome project

GGP HD150K SNP data for 5 breeds of Asian origin

This set includes autosomal genotypes for 3 Russian breeds of Asian origin on the GeneSeek HD150K SNP array (MAF<0.05): Kalmyk, Yakut, and Buryat combined with the sequence-based genotypes of Hanwoo and Illumina HD based genotypes of Japanese Black breeds

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

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