Urban particulate matter (PM) suppresses airway antibacterial defence.

Urban particulate matter (PM) suppresses airway antibacterial defence.
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城市颗粒物 (PM) 抑制气道抗菌防御

DOI:
10.1186/s12931-017-0700-0
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发表时间:
2018-01-08
影响因子:
5.8
通讯作者:
Pan J
Pan J
中科院分区:
医学2区
文献类型:
--
作者:
Chen X;Liu J;Zhou J;Wang J;Chen C;Song Y;Pan J

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背景流行病学研究表明,城市颗粒物(PM)增加了呼吸道感染的风险。然而,人们对其潜在的机制知之甚少。PM被认为可以抑制呼吸道上皮细胞对感染的天然防御反应的激活。用逆转录聚合酶链式反应和酶联免疫吸附试验检测抗菌肽水平。结果PM通过抑制呼吸道上皮细胞分泌抗菌素-2(β-Defensin-2,HBD-2)而增加细菌侵袭力,但不影响其他抗菌肽的分泌。PM进一步增加细菌诱导的ROS产生,同时伴随着细胞加速衰老和细菌诱导的HBD-2产生减少,抗氧化剂NAC处理减弱了这些影响。PM暴露可进一步上调IL-8的表达,但下调感染时IL-13的表达。结论PM通过抑制HBD-2氧化猝发诱导呼吸道上皮细胞的侵袭而促进细菌的侵袭。这些发现将PM与感染的易感性增加联系在一起。这些发现提供了关于颗粒物致病的潜在机制的洞察。
BackgroundEpidemiological studies have shown that urban particulate matter (PM) increases the risk of respiratory infection. However, the underlying mechanisms are poorly understood. PM has been postulated to suppress the activation of airway epithelial innate defence in response to infection.MethodsThe effects of PM on antibacterial defence were studied using an in vitro infection model. The levels of antimicrobial peptides were measured using RT-PCR and ELISA. In addition to performing colony-forming unit counts and flow cytometry, confocal microscopy was performed to directly observe bacterial invasion upon PM exposure.ResultsWe found that PM PM increased bacterial invasion by impairing the induction of β-defensin-2 (hBD-2), but not the other antimicrobial peptides (APMs) secreted by airway epithelium. PM further increases bacteria-induced ROS production, which is accompanied by an accelerated cell senescence and a decrease in bacteria-induced hBD-2 production, and the antioxidant NAC treatment attenuates these effects. The PM exposure further upregulated the expression of IL-8 but downregulated the expression of IL-13 upon infection.ConclusionsPM promotes bacterial invasion of airway epithelial cells by attenuating the induction of hBD-2 via an oxidative burst. These findings associate PM with an increased susceptibility to infection. These findings provide insight into the underlying mechanisms regarding the pathogenesis of particulate matter.
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