Biological material on inhaled coarse fraction particulate matter activates airway phagocytes in vivo in healthy volunteers.
BACKGROUND
In vitro, endotoxin on coarse fraction particulate matter (PM2.5-10) accounts for the majority of the ability of PM2.5-10 to induce cytokine responses from alveolar macrophages.


OBJECTIVE
We examined in vivo whether inhaled PM2.5-10 from local ambient air induce inflammatory and immune responses in the airways of healthy human beings and whether biologic material on PM2.5-10 accounts for these effects.


METHODS
On 3 separate visits, 9 healthy subjects inhaled nebulized saline (0.9%, control), PM2.5-10 collected from local ambient air that was heated to inactivate biological material (PM2.5-10-), or nonheated PM (PM2.5-10+). PM2.5-10 deposition (approximately 0.65 mg/subject) targeted the bronchial airways (confirmed by using radiolabeled aerosol), and induced sputum was obtained 2 to 3 hours postinhalation for analysis of cellular and biochemical markers of inflammation and innate immune function.


RESULTS
Inhaled PM2.5-10+ induced elevated inflammation (% PMNs, macrophage mRNA TNF-alpha), increased eotaxin, upregulated immune surface phenotypes on macrophages (mCD14, CD11b, HLA-DR), and increased phagocytosis (monocytes) versus saline (P < .05). Biological inactivation of PM2.5-10 (PM2.5-10-) had no effect on neutrophilia but significantly (P < .05) attenuated mRNA TNF-alpha, eotaxin levels, cell surface marker responses, and phagocytosis.


CONCLUSIONS
Biological components of PM2.5-10 are not necessary to induce neutrophil responses but are essential in mediating macrophage responses. The ability of PM2.5-10 to activate monocytic cells and potentially skew the airways toward an allergic phenotype by enhancing eotaxin levels may enhance responses to allergens or bacteria in individuals with allergy.


CONCLUSIONS
PM2.5-10 might enhance the response of individuals with allergy to airborne bacteria.
Alexis
Neil E
NE
Center for Environmental Medicine Asthma and Lung Biology, University of North Carolina at Chapel Hill, NC 27599-7310, USA. Neil_Alexis@med.unc.edu
Lay
John C
JC
Zeman
Kirby
K
Bennett
William E
WE
Peden
David B
DB
Soukup
Joleen M
JM
Devlin
Robert B
RB
Becker
Susanne
S
D000293:Adolescent; D000328:Adult; D000336:Aerosols; D000393:Air Pollutants / Q000276:immunology* / Q000494:pharmacology; D001980:Bronchi / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D005260:Female; D006801:Humans; D016130:Immunophenotyping; D019570:Inhalation Exposure; D008262:Macrophage Activation / Q000276:immunology*; D008297:Male; D018375:Neutrophil Activation / Q000276:immunology*; D010316:Particle Size; D010587:Phagocytosis / Q000276:immunology; D020545:Respiratory Mucosa / Q000166:cytology / Q000276:immunology*; D013183:Sputum / Q000166:cytology / Q000276:immunology / Q000378:metabolism
D000336:Aerosols; D000393:Air Pollutants