Interaction between respiratory syncytial virus and particulate matter in guinea pig alveolar macrophages
Interaction between respiratory syncytial virus and particulate matter in guinea pig alveolar macrophages
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DOI：
10.1165/rcmb.2002-0115oc
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发表时间：
2003-06-01
影响因子：
6.4
通讯作者：
Hegele, RG
中科院分区：
文献类型：
--
作者：
Kaan, PM;Hegele, RG
肺泡巨噬细胞（AM）在宿主肺防御机制中起着关键作用。呼吸道合胞病毒（RSV）刺激AM分泌促炎细胞因子，同时抑制细胞的吞噬能力。然而，已报道AM暴露于环境颗粒物（PM10）抑制RSV摄取。AM中RSV与PM 10相互作用的机制尚不清楚.我们假设AM对RSV和PM10的细胞反应依赖于AM暴露于这些试剂的顺序。在这项研究中，我们比较了RSV和PM10体外暴露对豚鼠AM吞噬功能、AM中RSV产量和促炎细胞因子（白细胞介素[IL]-6，IL-8和肿瘤坏死因子[TNF]-α）产生的顺序效应。连续暴露于RSV和PM 10对AM吞噬PM 10的能力没有影响。与未暴露于PM10的AM相比，无论暴露顺序如何，暴露于PM10的AM的RSV产量均严重降低（P < 0.004）。与对照组相比，AM暴露于RSV和/或PM 10导致生物活性TNF-α的分泌增加（P < 0.02），这些试剂对TNF-α的产生没有协同或抑制相互作用。与此相反，AM暴露于PM10显著降低RSV诱导的IL-6（P < 4 × 10 - 6）和IL-8（P < 0.003）的产生。总之，我们的研究结果表明，PM10暴露可能会干扰豚鼠AM中RSV复制和病毒诱导的细胞因子产生的机制，独立于暴露于这些药物的顺序。
Alveolar macrophages (AM) play a pivotal role in host lung defense mechanisms. Respiratory syncytial virus (RSV) stimulates secretion of proinflammatory cytokines in AM while it suppresses the cell's phagocytic ability. However, exposure of AM to ambient particulate matter (PM10) has been reported to inhibit RSV uptake. The mechanisms involved in the interaction between RSV and PM 10 in AM are not known. We hypothesize that the cellular response of AM to RSV and PM10 is dependent on the sequence in which AM are exposed to these agents. In this study, we compared the sequential effect of RSV and PM10 exposure in vitro on the phagocytic function of guinea pig AM, the RSV Yield in AM, and the production of proinflammatory cytokines (interleukin [IL]-6, IL-8, and tumor necrosis factor [TNF]-alpha). The ability of AM to phagocytose PM10 was not affected by sequential exposure to RSV and PM10. RSV Yield was severely decreased in PM10-exposed AM, regardless of sequence of exposure, compared with AM that were not exposed to PM10 (P < 0.004). Exposure of AM to RSV and/or PM10 resulted in enhanced secretion of bioactive TNF-alpha compared with controls (P < 0.02), without synergistic or inhibitory interaction of these agents on TNF-a production. By contrast, exposure of AM to PM10 significantly decreased the production of RSV-induced IL-6 (P < 4 x 10(-6)) and IL-8 (P < 0.003). In summary, our findings suggest that PM10 exposure may interfere with mechanisms of RSV replication and viral-induced cytokine production in guinea pig AM, independent of the sequence of exposure to these agents.