流感病毒继发细菌感染加重的免疫学机制研究进展

Research progress immunological mechanisms in exacerbation of secondary bacterial infection following influenza virus

流感病毒是发病率最高的呼吸道感染病原体之一,而流感病毒感染后易继发细菌感染导致细菌性肺炎,这也是流感流行期间导致死亡的主要原因,具有抗生素治疗有限、病情急性加重和预后差等特点。临床研究发现,即使轻症流感病毒感染后继发细菌感染也会诱导重症肺脏细菌性肺炎和损伤,从而导致死亡。研究表明多种免疫细胞和免疫相关分子的变化,以及二者的相互作用参与流感病毒致病机制。本文主要综述肺脏天然免疫细胞和细胞因子在流感病毒继发细菌感染加重中的作用机制,通过了解机体免疫应答在病毒和细菌之间的协同作用,将有助于寻找新的靶点并设计新的临床治疗方案,降低流感病毒继发细菌性肺炎的发生和发展。

Influenza virus is one of the pathogens with the highest incidence of respiratory infections. Influenza infection increased susceptibility to secondary bacterial infection,and then leading to bacterial pneumonia,which is also the main cause of death during the influenza epidemic. It has the characteristics of limited antibiotic treatment,acute exacerbation and poor prognosis. Clinical studies have found that even mild influenza infection,the secondary bacterial infection can also induce severe lung bacterial pneumonia and lung injury,leading to death. Current studies have shown that changes of multiple immune cells and associated immune molecules,as well as the interaction between them,are involved in the pathogenesis of influenza virus. Here,we mainly review the mechanisms by which innate immune cells and cytokines exacerbated bacterial infection which followed influenza infection in the lung,understanding the synergistic effect of immune responses between the virus and bacteria,will help to find novel targets,design new clinical therapeutic schedules and reduce the occurrence and development of secondary bacterial pneumonia with influenza.