Retired United States Patent and Trademark Office, San Jose, CA, USA.
J Infect Chemother. 2024 Oct;30(10):959-970. doi: 10.1016/j.jiac.2024.07.006. Epub 2024 Jul 6.
Respiratory viral infections, including respiratory syncytial virus (RSV), parainfluenza viruses and type A and B influenza viruses, can have severe outcomes. Bacterial infections frequently follow viral infections, and influenza or other viral epidemics periodically have higher mortalities from secondary bacterial pneumonias. Most secondary bacterial infections can cause lung immunosuppression by fatty acid mediators which activate cellular receptors to manipulate neutrophils, macrophages, natural killer cells, dendritic cells and other lung immune cells. Bacterial infections induce synthesis of inflammatory mediators including prostaglandins and leukotrienes, then eventually also special pro-resolving mediators, including lipoxins, resolvins, protectins and maresins, which normally resolve inflammation and immunosuppression. Concurrent viral and secondary bacterial infections are more dangerous, because viral infections can cause inflammation and immunosuppression before the secondary bacterial infections worsen inflammation and immunosuppression. Plausibly, the higher mortalities of secondary bacterial pneumonias are caused by the overwhelming inflammation and immunosuppression, which the special pro-resolving mediators might not resolve.
呼吸道病毒感染，包括呼吸道合胞病毒（RSV）、副流感病毒以及甲型和乙型流感病毒，可能导致严重后果。病毒感染后常继发细菌感染，流感或其他病毒流行期间，继发细菌性肺炎的死亡率更高。大多数继发细菌感染可通过脂肪酸介质引起肺部免疫抑制，这些介质激活细胞受体以操纵中性粒细胞、巨噬细胞、自然杀伤细胞、树突状细胞和其他肺部免疫细胞。细菌感染诱导合成炎症介质，包括前列腺素和白三烯，然后最终还包括特殊的促解决介质，包括脂氧素、解析素、保护素和maresin，这些介质通常可解决炎症和免疫抑制。同时发生的病毒和继发细菌感染更危险，因为病毒感染可在继发细菌感染加重炎症和免疫抑制之前引起炎症和免疫抑制。合理的是，继发细菌性肺炎的高死亡率是由过度的炎症和免疫抑制引起的，而特殊的促解决介质可能无法解决这些问题。
