Coarse (PM2.5-10), fine (PM2.5), and ultrafine air pollution particles induce/increase immune costimulatory receptors on human blood-derived monocytes but not on alveolar macrophages

Diesel particles have been shown to possess adjuvant activity and influence the development of allergic sensitization. Also, more heterogeneous mixtures of pollution particles have been shown to affect host defenses and development of immunity in animal models. in the present study it was determined whether freshly collected particulate matter (PM10) in the size ranges 2.5-10 mum (PM2.5-10, coarse), 0.1-2.5 mum (PM2.5, fine), and less than or equal to0.1 mum (ultrafine) in diameter affected the development of antigen presenting cells by evaluating the expression of surface receptors involved in T-cell interaction on both human alveolar macrophages (AM) and blood-derived monocytes (Mo). A Mo-AM coculture was exposed to 50 mug/ml of particles and expression of HLA-DR, CD40, CD80, and CD86 on each cell type was assessed by flow cytometry. Mo upregulated the expression of all four receptors in response to each of the particle fractions, while expression was unaffected in AM. The cells were also exposed to two model air pollution particles, diesel dust and volcanic ash, neither of which affected receptor expression. Furthermore, Mo and AM were separately exposed to the three PM size fractions and supernatants assessed for the T-helper (CD4(+)) lymphocyte chemoattractant interleukin-16 (IL-16). AM, but not Mo, produced IL-16, and this chemoattractant was released only in response to PM2.5-10. These data suggest that a wide size range of pollution particles contain materials that may promote antigen presentation by Mo, while the capability to specifically recruit CD4(+) lymphocytes is contained in AM stimulated with the coarse PM fraction.