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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Differentiated human alveolar type II cells secrete antiviral IL-29 (IFN-lambda1) in response to influenza A infection.
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Differentiated human alveolar type II cells secrete antiviral IL-29 (IFN-lambda1) in response to influenza A infection.

机译：分化的人类II型肺泡细胞在对A型流感感染后会分泌抗病毒IL-29（IFN-lambda1）。

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摘要

Alveolar type II epithelial cells (ATIIs) are one of the primary targets for influenza A pneumonia. The lack of a culture system for maintaining differentiated ATIIs hinders our understanding of pulmonary innate immunity during viral infection. We studied influenza A virus (IAV)-induced innate immune responses in differentiated primary human ATIIs and alveolar macrophages (AMs). Our results indicate that ATIIs, but not AMs, support productive IAV infection. Viral infection elicited strong inflammatory chemokine and cytokine responses in ATIIs, including secretion of IL-8, IL-6, MCP-1, RANTES, and MIP-1beta, but not TNF-alpha, whereas AMs secreted TNF-alpha as well as other cytokines in response to infection. Wild-type virus A/PR/8/34 induced a greater cytokine response than reassortant PR/8 virus, A/Phil/82, despite similar levels of replication. IAV infection increased mRNA expression of IFN genes IFN-beta, IL-29 (IFN-lambda1), and IL-28A (IFN-lambda2). The major IFN protein secreted by type II cells was IL-29 and ATIIs appear to be a major resource for production of IL-29. Administration of IL-29 and IFN-beta before infection significantly reduced the release of infectious viral particles and CXC and CC chemokines. IL-29 treatment of type II cells induced mRNA expression of antiviral genes MX1, OAS, and ISG56 but not IFN-beta. IL-29 induced a dose-dependent decrease of viral nucleoprotein and an increase of antiviral genes but not IFN-beta. These results suggest that IL-29 exerts IFN-beta-independent protection in type II cells through direct activation of antiviral genes during IAV infection.
机译：II型肺泡上皮细胞（ATIIs）是A型流感肺炎的主要靶标之一。缺乏用于维持分化的ATII的培养系统，阻碍了我们对病毒感染过程中肺先天免疫的理解。我们研究了甲型流感病毒（IAV）诱导的先天性免疫应答在分化的主要人类ATII和肺泡巨噬细胞（AM）中的作用。我们的结果表明，ATII（而非AM）支持生产性IAV感染。病毒感染在ATII中引起强烈的炎症趋化因子和细胞因子反应，包括IL-8，IL-6，MCP-1，RANTES和MIP-1beta的分泌，但不分泌TNF-α，而AM分泌TNF-α和其他对感染有反应的细胞因子。尽管复制水平相似，但野生型病毒A / PR / 8/34诱导的细胞因子反应比重配的PR / 8病毒A / Phil / 82更大。 IAV感染会增加IFN基因IFN-beta，IL-29（IFN-lambda1）和IL-28A（IFN-lambda2）的mRNA表达。 II型细胞分泌的主要IFN蛋白是IL-29，而ATII似乎是产生IL-29的主要资源。感染前给予IL-29和IFN-β可显着降低感染性病毒颗粒以及CXC和CC趋化因子的释放。 IL-29处理II型细胞可诱导抗病毒基因MX1，OAS和ISG56的mRNA表达，但不能诱导IFN-β的表达。 IL-29诱导病毒核蛋白的剂量依赖性降低和抗病毒基因的升高，但不诱导IFN-β。这些结果表明，IL-29在IAV感染过程中通过直接激活抗病毒基因在II型细胞中发挥IFN-β独立的保护作用。

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