Biological material on inhaled coarse fraction particulate matter activates airway phagocytes in vivo in healthy volunteers - 20/08/11
, John C. Lay, DVM, PhD a, Kirby Zeman, PhD a, William E. Bennett, PhD a, David B. Peden, MD, MS a, Joleen M. Soukup, MPH b, Robert B. Devlin, PhD b, Susanne Becker, PhD b
Reprint requests: Neil E. Alexis, MHSc, PhD, Center for Environmental Medicine, Asthma and Lung Biology, UNC Chapel Hill, Chapel Hill, NC 27599-7310.Chapel Hill, NC
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 (
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-⍺), 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-⍺, eotaxin levels, cell surface marker responses, and phagocytosis.
Conclusion |
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.
Clinical implications |
PM2.5-10 might enhance the response of individuals with allergy to airborne bacteria.
Le texte complet de cet article est disponible en PDF.Key words : PM2.5-10, airway macrophages, TNF-⍺, mCD14, eotaxin
Abbreviations used : C, Mac, MFI, MMAD, P, PM, PM2.5-10, PM10, ROI, SC, TLR
Plan
| Environmental Protection Agency Disclaimer: The research described in this article has been funded wholly or in part by the United States Environmental Protection Agency through cooperative agreement CR829522 with the Center for Environmental Medicine, Asthma and Lung Biology at the University of North Carolina at Chapel Hill. However, it does not necessarily reflect the views of the agency, and no official endorsement should be inferred. Mention of trade names or commercial products does not constitute endorsement or recommendation for use. Supported by RO1HL-62624, RO1 HL 66559US EPA, and CR-829522. Disclosure of potential conflict of interest: D. Peden has consultant arrangements with Genentech/Novartis, GSK, and Merck; receives grant support from Genentech/Novartis and GSK; and is on the speakers’ bureau for GSK and Sepracor. R. Devlin is employed by the US Environmental Protection Agency. The rest of the authors have declared that they have no conflict of interest. |
Vol 117 - N° 6
P. 1396-1403 - juin 2006 Retour au numéro
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