title: Biological material on inhaled coarse fraction particulate matter activates airway phagocytes in vivo in healthy volunteers.
abstract: 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.
authors.affiliation: Center for Environmental Medicine Asthma and Lung Biology, University of North Carolina at Chapel Hill, NC 27599-7310, USA. Neil_Alexis@med.unc.edu
authors.forename: Neil E
authors.initials: NE
authors.lastname: Alexis
authors.forename: John C
authors.initials: JC
authors.lastname: Lay
authors.forename: Kirby
authors.initials: K
authors.lastname: Zeman
authors.forename: William E
authors.initials: WE
authors.lastname: Bennett
authors.forename: David B
authors.initials: DB
authors.lastname: Peden
authors.forename: Joleen M
authors.initials: JM
authors.lastname: Soukup
authors.forename: Robert B
authors.initials: RB
authors.lastname: Devlin
authors.forename: Susanne
authors.initials: S
authors.lastname: Becker
mesh_terms: 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
chemical_list: D000336:Aerosols; D000393:Air Pollutants