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J Virol:白细胞介素-22可保护机体抵御流感后细菌的二次感染

来源:生物谷 2013-06-03 00:21

2013年6月3日 讯 /生物谷BIOON/ --近日,来自巴斯德研究院的研究者通过对小鼠模型进行研究揭示了,白细胞介素-22(IL-22)可以保护小鼠模型抵御细菌的二次感染,这种二次感染可由流行性感冒再度引起。相关研究成果刊登于国际病毒学杂志Journal of Virology上。

A型流感病毒感染可以导致原发型肺炎,而后会引发严重的并发症,包括二度细菌性肺炎以及败血症。在季节性流行病以及大范围流行病期间,流感病毒流行后的细菌二度感染的发生是人类健康的一大健康隐患,而且可能会引发严重的社会经济负担。

研究者Francois Trottein表示,能够理解流感后细菌的二次感染对于开发相应抑制方法非常关键,对小鼠的研究揭示了,宿主先天免疫系统的损伤以及病毒引发的肺损伤都是细菌二次感染的主要特征,研究者还检测了一种假设,就是IL-22是否在流感期间扮演着重要角色。

在文中,研究者表示,属于先天免疫系统的许多细胞类型都可以在感染之后产生IL-22,缺少IL-22可以加速肺部病症的恶化以及上皮组织的损伤。而且内生的IL-22在小鼠免疫系统的二次感染中扮演着保护性的角色。

尽管IL-22维持保护性效应的机制尚不清楚,研究者推测这种有益的作用可能来自于其在上皮完整性维持方面扮演的角色。最后研究者表示,如果IL-22在人类机体也发挥着功能,那么IL-22的产生也将会给流感患者带持续性的益处。(生物谷Bioon.com)

Interleukin-22 Reduces Lung Inflammation during Influenza A Virus Infection and Protects against Secondary Bacterial Infection

Stoyan Ivanova,b,c,d,e*, Joelle Rennesona,b,c,d,e, Josette Fontainea,b,c,d,e, Adeline Barthelemya,b,c,d,e, Christophe Pageta,b,c,d,e, Elodie Macho Fernandeza,b,c,d,e, Fany Blancf,g, Carl De Trezh, Laurye Van Maelea,b,c,d,e, Laure Dumoutieri, Michel-René Huerref,j, Gérard Eberlf,k, Mustapha Si-Taharf,g, Pierre Gossetl, Jean Christophe Renauldi, Jean Claude Sirarda,b,c,d,e, Christelle Faveeuwa,b,c,d,e and François Trotteina,b,c,d,e

Interleukin-22 (IL-22) has redundant, protective, or pathogenic functions during autoimmune, inflammatory, and infectious diseases. Here, we addressed the potential role of IL-22 in host defense and pathogenesis during lethal and sublethal respiratory H3N2 influenza A virus (IAV) infection. We show that IL-22, as well as factors associated with its production, are expressed in the lung tissue during the early phases of IAV infection. Our data indicate that retinoic acid receptor-related orphan receptor-γt (RORγt)-positive αβ and γδ T cells, as well as innate lymphoid cells, expressed enhanced Il22 transcripts as early as 2 days postinfection. During lethal or sublethal IAV infections, endogenous IL-22 played no role in the control of IAV replication and in the development of the IAV-specific CD8+ T cell response. During lethal infection, where wild-type (WT) mice succumbed to severe pneumonia, the lack of IL-22 did not accelerate or delay IAV-associated pathogenesis and animal death. In stark contrast, during sublethal IAV infection, IL-22-deficient animals had enhanced lung injuries and showed a lower airway epithelial integrity relative to WT littermates. Of importance, the protective effect of endogenous IL-22 in pulmonary damages was associated with a more controlled secondary bacterial infection. Indeed, after challenge with Streptococcus pneumoniae, IAV-experienced Il22−/− animals were more susceptible than WT controls in terms of survival rate and bacterial burden in the lungs. Together, IL-22 plays no major role during lethal influenza but is beneficial during sublethal H3N2 IAV infection, where it limits lung inflammation and subsequent bacterial superinfections.

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