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Polymorphonuclear leukocytes (PMNs) are among the first responders in the lung following pneumococcal infection and are required for bacterial clearance. However, PMN antimicrobial function declines with age. To identify mechanisms underlying this decline, we performed RNA sequencing on PMNs in the lungs of young and old mice following pulmonary infection with\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>S.\u2009pneumoniae<\/jats:italic>\n                    <\/jats:styled-content>\n                    . We observed significant transcriptomic differences across host age. Transcriptional analysis followed by functional validation revealed that in infected mice, PMNs from aged hosts failed to upregulate several effector activities including glycolysis and subsequent mitochondrial reactive oxygen species (ROS) production, which are necessary for bacterial killing by PMNs. Conversely, PMNs in aged mice displayed a higher senescence\u2010associated secretory phenotype (SASP) score and upregulated pathways involved in cellular senescence. Follow\u2010up functional characterization found that in uninfected hosts, PMNs in aged mice expressed higher levels of SASP factors IL\u201010, TNF\u03b1, and ROS, had a lower incidence of apoptosis, and had a higher proportion of cells positive for senescence\u2010associated \u03b2\u2010galactosidase, features of a senescent\u2010like phenotype. Importantly, blocking TNF\u03b1, one of the SASP factors, altered the senescent\u2010like phenotype and boosted the antibacterial activity of PMNs from aged hosts and increased host resistance to\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>S.\u2009pneumoniae<\/jats:italic>\n                    <\/jats:styled-content>\n                    pulmonary infection. In conclusion, host aging is associated with altered PMN phenotype, including a shift toward senescent\u2010like energy\u2010deficient cells, which contribute to impaired host defense and represent potential targets for improved interventions against infection in older adults.\n                  <\/jats:p>","DOI":"10.1111\/acel.70435","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T18:24:40Z","timestamp":1772994280000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Host Aging Induces a Senescent\u2010Like Phenotype in Neutrophils and Altered Transcriptional Responses to\n                    <i>Streptococcus pneumoniae<\/i>"],"prefix":"10.1111","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4809-7991","authenticated-orcid":false,"given":"Michael C.","family":"Battaglia","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology 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