Ki-67 promotes inflammatory signaling governing neutrophil recruitment during respiratory infections

ABSTRACT: Neutrophils defend against respiratory infections but cause acute lung injury (ALI) when excessively recruited to the lung. Early life environmental factors can shape lung development, but how they impact neutrophil recruitment is not known. We show that exposing newborn mice to hyperoxia increases the number of adult alveolar type 1 (AT1) epithelial cells expressing the proliferation marker Ki-67. Although these cells were not proliferating, they express high levels of chemokines that stimulate neutrophil recruitment and ALI when mice were infected with influenza A virus or exposed to lipopolysaccharide (LPS). Neutrophil recruitment and chemokine production were attenuated in Ki-67 hypomorph mice infected with virus or exposed to LPS and enhanced by genetically over-expressing Ki-67 in th

ORGANISM(S): Mus musculus (mouse)

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PROVIDER: S-BSST1960 | biostudies-other |

REPOSITORIES: biostudies-other