Indoor Air Pollutants Stimulate Interleukin-8-Specific mRNA Expression and Protein Secretion of Alveolar Macrophages

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.

Pulmonary Exposure to Particles during Pregnancy Causes Increased Neonatal Asthma Susceptibility

“…For example, specially coated TiO 2 particles were shown to cause pulmonary inflammation (31). Moreover, TiO 2 particles were shown to cause pulmonary inflammation with activation of antigen-presenting cells and production of certain chemokines (32,33). They were also associated with increased production of IL-13 by mast cells (34) and, potentially germane to our study, were shown to cause increase IL-25 and IL-13 production by lung antigen-presenting cells (35).…”

Estrogen-mediated impairment of macrophageal uptake of environmental TiO2particles to explain inflammatory effect of TiO2on airways during pregnancy

“…when specially coated (Warheit et al, 2005). To add, TiO 2 particles were shown to induce pulmonary inflammation with activation of antigen-presenting cells (APC) and production of certain chemokines (Drumm et al, 1999;Renwick et al, 2004) and cytokines Kang et al, 2005).…”

Soot-Exposed Mononuclear Cells Increase Inflammatory Cytokine mRNA Expression and Protein Secretion in Cocultured Bronchial Epithelial Cells

“…IL-4 and IL-10 [25, 26]. It is known that particle-induced pathomechanisms involve chemotactic, proinflammatory or fibrogenic cytokines [28]. In this study, we attempted to determine the role of IL-6 and IL-8 in the autocrine stimulation of both cytokines in neighboring bronchial epithelial cells and monocytes following exposure to soot particles.…”

“…Inert particles (e.g. TiO 2 ) indeed stimulate cells of the monocyte lineage, albeit to a much lesser extent than soot particles or asbestos fibers [28, 29]. …”