The effects of senescence on geriatric disorders are well explored, but how it influences infections in the elderly is poorly addressed. Here, we show that several anti-microbial responses are elevated in senescent epithelial cells and old mice, which results in decreased bacterial survival in the host after infection. We identify higher levels of iNOS as a crucial host response and show that p38 MAPK in senescent epithelial cells acts as a negative regulator of iNOS transcription. However, in older mice, the ability to impede bacterial infection does not result in enhanced survival, possibly because elevated pro-inflammatory responses are not countered by a robust host protective anti-inflammatory response. Overall, while addressing an alternate advantage of senescent cells, our study demonstrates that infection-associated morbidity in the elderly may not be the sole outcome of pathogen loads but may also be influenced by the host's ability to resolve inflammation-induced damage.

衰老对老年疾病的影响得到了很好的探讨，但它如何影响老年人感染的问题却鲜为人知。在这里，我们表明衰老的上皮细胞和老年小鼠中的几种抗微生物反应升高，这导致感染后宿主中细菌存活率降低。我们将更高水平的 iNOS 确定为关键的宿主反应，并表明衰老上皮细胞中的 p38 MAPK 充当 iNOS 转录的负调节因子。然而，在老年小鼠中，阻止细菌感染的能力不会提高存活率，这可能是因为增强的促炎反应没有被强大的宿主保护性抗炎反应所抵消。总的来说，在解决衰老细胞的另一个优势的同时，