Ambient Pm10 Extracts Inhibit Phagocytosis Of Defined Inert Model Particles By Alveolar Macrophages

We used inert melamin particles that are very well defined in size (diameters: 0.5, 1.9, 6.8 mum) to study the effects of ambient particles of <10 mu m (PM10) on phagocytosis. Dose-response functions were found between the amount of added melamin particle mass and the toxicity. Fine particles (0.5 mu m) were more toxic at low and medium amounts of mass per cell added than the larger particles (1.9, 6.8 mu m). However, with regard to particle numbers applied per cell, toxicity is reversed, with the largest particles being the most toxic. In the whole dose range tested, the melamin particles used did not stimulate cells to produce oxidative radicals or tumor necrosis factor-alpha (TNF alpha). Flow cytometric analyses visualized the time-dependent melamin particle uptake, which was inhibited by polyinosinic acid ( Poly-I), suggesting that phagocytosis is mediated by scavenger-type receptors. Cells exposed to an aqueous PM10 extract, which also had a dose-dependent toxic potential, were stimulated to produce oxidative radicals, measured as NO2-, and TNFalpha. Combined exposures with the PM10 extract followed by the inert melamin particles show that the PM10 extract inhibits inert particle uptake by alveolar macrophages. It is proposed that ambient PM10, besides being toxic for alveolar macrophages, stimulates them to produce oxidative radicals and the proinflammotry cytokine TNFalpha. Moreover, it inhibits their particle uptake potential. Thus PM10 appears to promote inflammation and reduce defense.