Indoor air pollutants stimulate interleukin-8-specific mRNA expression and protein secretion of alveolar macrophages
Indoor air pollutants stimulate interleukin-8-specific mRNA expression and protein secretion of alveolar macrophages
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作者：
Drumm, K;Schindler, H;Kienast, K
室内空气污染物可引起气道和邻近肺组织的炎症性变化。在吞噬吸入颗粒后，肺泡巨噬细胞（AM）释放能够吸引炎性细胞进入肺组织的趋化介质。为了进一步评价这些机制，将外周血单核细胞（PBMNC）和人AM（从下呼吸道新鲜回收）暴露于室内颗粒Soot FR 101和Printer 90、石棉纤维温石棉B和浓度为10或50 μ g/10（6）个细胞的二氧化钛（TiO 2）中长达8小时。在Boyden小室中通过趋化性测定来定量粒细胞向AM和PBMNC的条件上清液中的迁移。粒细胞迁移增加42.3 +/- 25.8%（温石棉B）、64.6 +/- 18.3%（FR 101）、74.2 +/- 16.5%（P 90）和86.7 +/- 25.6%（TiO 2）用温石棉B、FR 101、P 90、和TiO 2，浓度为10和50 μ g/10（6）个细胞，持续90分钟。与未暴露的对照相比，在颗粒暴露后，每种测试颗粒均引起AM或PBMNC的IL-8特异性mRNA表达增加。为了确定是否涉及最强的粒细胞趋化因子IL-8，将上清液与抗IL-8预孵育。在AM条件化的上清液中，粒细胞迁移减少高达35 +/-15%（50 ng/ml抗IL-8）和41.5 +/-16%（100 ng/ml抗IL-8）（p < 0.0625）。用人IL-8预处理的粒细胞在AM条件化的上清液中减少高达59 +/-18%（10 ng/ml）（p < 0.0625）。使用抗IL-8预处理的颗粒暴露的PBMNC的上清液观察到类似的反应模式。总之，室内空气污染物可能通过肺泡巨噬细胞释放IL-8促进肺部炎症变化。
Indoor air pollutants may cause inflammatory changes of the airways and adjacent pulmonary tissue. After phagocytosis of inhaled particles alveolar macrophages (AM) release chemotactic mediators capable of attracting inflammatory cells into the lung tissue. To evaluate these mechanisms further peripheral blood mononuclear cells (PBMNC) and human AM (freshly recovered from the lower respiratory tract) were exposed to the indoor particles Soot FR 101 and Printer 90, the asbestos fiber Chrysotile B, and titanium dioxide (TiO2) at concentrations of 10 or 50 mu g/10(6) cells for up to 8 h. The migration of granulocytes into the conditioned supernatants of AM and PBMNC was quantified by chemotaxis assay in a Boyden chamber. Granulocyte migration increased by 42.3 +/- 25.8% (Chrysotile B), 64.6 +/- 18.3% (FR 101), 74.2 +/- 16.5% (P 90), and 86.7 +/- 25.6% (TiO2) in AM-conditioned supernatants (p < 0.05), Qualitative, Interleukin (IL)-8 specific reverse transcriptase-polymerase chain reaction was performed after exposure of AM or PBMNC to Chrysotile B, FR 101, P 90, and TiO2 at concentrations of 10 and 50 mu g/10(6) cells for 90 min. Each of the tested particles caused an increase in IL-8-specific mRNA expression of AM or PBMNC after particle exposure compared with the unexposed control. To find out if IL-8, the most powerful granulocyte chemokine, is involved, supernatants were preincubated with anti-IL-8. Granulocyte migration decreased by up to 35 +/- 15% (50 ng/ml anti-IL-8) and 41.5 +/- 16% (100 ng/ml anti-IL-8) (p < 0.0625) in AM-conditioned supernatants. Pretreatment of the granulocytes with human IL-8 decreased by up to 59 +/- 18% (10 ng/ml) (p < 0.0625) in AM-conditioned supernatants, Similar reaction patterns were observed using anti-IL-8-pretreated supernatants of particle-exposed PBMNC. In conclusion, indoor air pollutants may promote inflammatory changes in the lung via IL-8 release by alveolar macrophages.