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Indoor air pollutants stimulate interleukin-8-specific mRNA expression and protein secretion of alveolar macrophages
1IIIrd Department of Internal Medicine, Division of Pneumology, Johannes Gutenberg University Hospital, D-55131 Mainz, Germany.
Abstract:
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 Printex 90, the asbestos fiber Chrysotile B, and titanium dioxide (TiO2) at concentrations of 10 or 50 microg/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 microg/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.
Insights
Indoor air pollutants like soot and asbestos trigger lung inflammation by stimulating alveolar macrophages (AM) to release Interleukin-8 (IL-8). This IL-8 attracts inflammatory cells, worsening airway damage.
Area of Science:
- Pulmonary Medicine
- Immunology
- Environmental Health
Background:
- Indoor air pollutants can induce airway inflammation.
- Alveolar macrophages (AM) play a key role in lung inflammatory responses.
- Particle inhalation leads to the release of chemotactic mediators from AM.
Purpose of the Study:
- To investigate the inflammatory mechanisms induced by indoor air pollutants.
- To evaluate the role of Interleukin-8 (IL-8) in particle-induced lung inflammation.
- To assess the effect of specific indoor particles on AM and peripheral blood mononuclear cells (PBMNC).
Main Methods:
- Human AM and PBMNC were exposed to indoor particles (Soot FR 101, Printex 90, Chrysotile B, TiO2).
- Chemotaxis assays were used to quantify granulocyte migration into conditioned cell supernatants.
- Reverse transcriptase-polymerase chain reaction (RT-PCR) measured IL-8 mRNA expression.
- Neutralizing antibodies against IL-8 were used to confirm IL-8's role.
Main Results:
- Exposure to tested particles significantly increased granulocyte migration in AM-conditioned supernatants.
- All tested particles elevated IL-8 specific mRNA expression in AM and PBMNC.
- Neutralization of IL-8 reduced granulocyte migration, confirming IL-8's involvement.
Conclusions:
- Indoor air pollutants promote lung inflammation through IL-8 release by alveolar macrophages.
- IL-8 is a key mediator in the inflammatory cascade initiated by inhaled particles.
- These findings highlight the respiratory health risks associated with indoor air quality.