Host Aging Induces a Senescent-Like Phenotype in Neutrophils and Altered Transcriptional Responses to Streptococcus pneumoniae - PubMed
8 hours ago
- #aging
- #neutrophils
- #pneumonia
- Aging increases susceptibility to respiratory infections by Streptococcus pneumoniae.
- Polymorphonuclear leukocytes (PMNs) are crucial for bacterial clearance but their function declines with age.
- RNA sequencing revealed significant transcriptomic differences in PMNs between young and old mice infected with S. pneumoniae.
- PMNs from aged hosts failed to upregulate glycolysis and mitochondrial ROS production, essential for bacterial killing.
- Aged PMNs exhibited higher senescence-associated secretory phenotype (SASP) scores and upregulated cellular senescence pathways.
- Uninfected aged PMNs showed higher levels of SASP factors (IL-10, TNFα, ROS), lower apoptosis, and more senescence-associated β-galactosidase-positive cells.
- Blocking TNFα improved PMN antibacterial activity and host resistance to S. pneumoniae in aged mice.
- Aging shifts PMNs toward a senescent-like, energy-deficient phenotype, impairing host defense.