Parker Dane
Department of Pediatrics, Columbia University, New York.
J Infect Dis. 2017 Feb 15;215(suppl_1):S58-S63. doi: 10.1093/infdis/jiw466.
The increased morbidity and mortality associated with bacterial pneumonias that are acquired following influenza infection are well appreciated by clinicians. One of the major components of the immune response to influenza is the induction of the types I and III interferon cascades, which encompasses the activation of over 300 genes. The immunological consequences of IFN activation, while important for viral clearance, modify the host proinflammatory responses through effects on the inflammasome, Th17 signaling and recruitment of phagocytic cells. IFN signaling affects both susceptibility to subsequent Streptococcus pneumoniae and Staphylococcus aureus infection as well as the intensity of the immune responses associated with pulmonary damage. Appreciation for the effects of IFN activation on anti-bacterial pulmonary defense mechanisms should help to inform therapeutic strategies in an ICU setting.
临床医生充分认识到流感感染后获得性细菌性肺炎相关的发病率和死亡率增加。对流感免疫反应的主要组成部分之一是I型和III型干扰素级联反应的诱导，这涉及300多个基因的激活。IFN激活的免疫后果虽然对病毒清除很重要，但通过对炎性小体、Th17信号传导和吞噬细胞募集的影响来改变宿主促炎反应。IFN信号传导既影响对随后肺炎链球菌和金黄色葡萄球菌感染的易感性，也影响与肺损伤相关的免疫反应强度。认识到IFN激活对肺部抗菌防御机制的影响应有助于为重症监护病房的治疗策略提供参考。
