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Ambient PM(10) extracts inhibit phagocytosis of defined inert model particles by alveolar macrophages
Christian Monn1, Roman Fendt, Theo Koller
1Institute for Hygiene and Applied Physiology, Group of Environmental Hygiene, Federal Institute of Technology, Zürich, Switzerland. monn@iha.bepr.ethz.ch
Abstract:
We used inert melamin particles that are very well defined in size (diameters: 0.5, 1.9, 6.8 microm) to study the effects of ambient particles of <10 microm (PM(10)) on phagocytosis. Dose-response functions were found between the amount of added melamin particle mass and the toxicity. Fine particles (0.5 microm) were more toxic at low and medium amounts of mass per cell added than the larger particles (1.9, 6.8 microm). 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 PM(10) extract, which also had a dose-dependent toxic potential, were stimulated to produce oxidative radicals, measured as NO(2)(-), and TNF alpha. Combined exposures with the PM(10) extract followed by the inert melamin particles show that the PM(10) extract inhibits inert particle uptake by alveolar macrophages. It is proposed that ambient PM(10), besides being toxic for alveolar macrophages, stimulates them to produce oxidative radicals and the proinflammotry cytokine TNF alpha. Moreover, it inhibits their particle uptake potential. Thus PM(10) appears to promote inflammation and reduce defense.
Insights
Fine particles (<10 microm) are more toxic to lung cells than larger ones, but particle number, not mass, determines toxicity. Ambient PM(10) exposure promotes inflammation and impairs lung defense mechanisms.
Area of Science:
- Environmental Health
- Toxicology
- Cell Biology
Background:
- Ambient particulate matter (PM(10)) poses a significant threat to respiratory health.
- Understanding the specific mechanisms of PM(10) toxicity and its impact on lung cell function is crucial.
Purpose of the Study:
- To investigate the effects of particle size and dose on the toxicity and phagocytosis of inert particles by alveolar macrophages.
- To elucidate the impact of ambient PM(10) extracts on cellular responses, including oxidative stress and inflammatory cytokine production.
- To determine how PM(10) exposure influences the phagocytic capacity of alveolar macrophages.
Main Methods:
- Utilized inert melamine particles of defined sizes (0.5, 1.9, 6.8 microm) to assess dose-response toxicity and phagocytosis.
- Employed flow cytometry to visualize time-dependent particle uptake and identify mediating receptors.
- Exposed cells to aqueous PM(10) extracts to measure oxidative radical and TNF-alpha production.
Main Results:
- Smaller melamine particles (0.5 microm) were more toxic per cell mass, while larger particles were more toxic per particle number.
- Melamine particles did not induce oxidative radicals or TNF-alpha, but their uptake was mediated by scavenger receptors.
- PM(10) extracts induced oxidative radicals and TNF-alpha, and inhibited melamine particle uptake by macrophages.
Conclusions:
- Ambient PM(10) is toxic to alveolar macrophages, inducing oxidative stress and TNF-alpha production.
- PM(10) exposure impairs the phagocytic defense function of alveolar macrophages.
- These effects suggest that PM(10) promotes inflammation and compromises lung defense mechanisms.
