Host responses to S. pneumoniae in wild type and Mertk mutant mice.

ABSTRACT: Streptococcus pneumoniae is the leading cause of community-acquired pneumonia. Mertk is a receptor tyrosine kinase and a member of the TAM family. It serves as an efferocytosis receptor involved in the recognition and removal of apoptotic debris by phagocytic cells, dampening the inflammatory response. Here we show that at 24h post-inoculation with S. pneumoniae, Mertk-/- mice generated through homologous recombination and backcrossed (HRB-Mertk-/- mice) have fewer bacteria present in their pneumonic lung than wild type mice. This enhanced clearance was not observed in Mertk-/- mice generated by CRISPR technology. The enhanced clearance of HRB-Mertk-/- mice was associated with fewer neutrophils and more IFNγ in the bronchoalveolar lavage, but was not prevented by a neutralizing IFNγ antibo

SUBMITTER: McPeek MK 

PROVIDER: S-EPMC12002534 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature