PMID- 20540623 OWN - NLM STAT- MEDLINE DCOM- 20101013 LR - 20211020 IS - 1091-7691 (Electronic) IS - 0895-8378 (Print) IS - 0895-8378 (Linking) VI - 22 IP - 8 DP - 2010 Jul TI - Comparative airway inflammatory response of normal volunteers to ozone and lipopolysaccharide challenge. PG - 648-56 LID - 10.3109/08958371003610966 [doi] AB - Ozone and lipopolysaccharide (LPS) are environmental pollutants with adverse health effects noted in both healthy and asthmatic individuals. The authors and others have shown that inhalation of ozone and LPS both induce airway neutrophilia. Based on these similarities, the authors tested the hypothesis that common biological factors determine response to these two different agents. Fifteen healthy, nonasthmatic volunteers underwent a 0.4 part per million ozone exposure for 2 h while performing intermittent moderate exercise. These same subjects underwent an inhaled LPS challenge with 20,000 LPS units of Clinical Center Reference LPS, with a minimum of 1 month separating these two challenge sessions. Induced sputum was obtained 24 h before and 4-6 h after each exposure session. Sputum was assessed for total and differential cell counts and expression of cell surface proteins as measured by flow cytometry. Sputum supernatants were assayed for cytokine concentration. Both ozone and LPS challenge augmented sputum neutrophils and subjects' responses were significantly correlated (R = .73) with each other. Ozone had greater overall influence on cell surface proteins by modifying both monocytes (CD14, human leukocyte antigen [HLA]-DR, CD11b) and macrophages (CD11b, HLA-DR) versus LPS where CD14 and HLA-DR were modified only on monocytes. However, LPS significantly increased interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha, with no significant increases seen after ozone challenge. Ozone and LPS exposure in healthy volunteers induce similar neutrophil responses in the airways; however, downstream activation of innate immune responses differ, suggesting that oxidant versus bacterial air pollutants may be mediated by different mechanisms. FAU - Hernandez, Michelle L AU - Hernandez ML AD - Department of Pediatrics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7310, USA. michelle_hernandez@med.unc.edu FAU - Harris, Bradford AU - Harris B FAU - Lay, John C AU - Lay JC FAU - Bromberg, Philip A AU - Bromberg PA FAU - Diaz-Sanchez, David AU - Diaz-Sanchez D FAU - Devlin, Robert B AU - Devlin RB FAU - Kleeberger, Steven R AU - Kleeberger SR FAU - Alexis, Neil E AU - Alexis NE FAU - Peden, David B AU - Peden DB LA - eng GR - P30 ES010126/ES/NIEHS NIH HHS/United States GR - UL1RR025746/RR/NCRR NIH HHS/United States GR - R01 ES012706/ES/NIEHS NIH HHS/United States GR - KL2 RR025746/RR/NCRR NIH HHS/United States GR - KL2RR025746/RR/NCRR NIH HHS/United States GR - R01 ES012706-05/ES/NIEHS NIH HHS/United States GR - R01ES012706/ES/NIEHS NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, U.S. Gov't, Non-P.H.S. PL - England TA - Inhal Toxicol JT - Inhalation toxicology JID - 8910739 RN - 0 (Air Pollutants) RN - 0 (HLA-DR Antigens) RN - 0 (Interleukins) RN - 0 (Lipopolysaccharide Receptors) RN - 0 (Lipopolysaccharides) RN - 0 (Tumor Necrosis Factor-alpha) RN - 66H7ZZK23N (Ozone) SB - IM MH - Administration, Inhalation MH - Adult MH - Air Pollutants/immunology/toxicity MH - Female MH - HLA-DR Antigens/metabolism MH - Humans MH - Immunity, Innate/drug effects MH - Interleukins/metabolism MH - Lipopolysaccharide Receptors/metabolism MH - Lipopolysaccharides/administration & dosage/immunology/*toxicity MH - Macrophages/drug effects/metabolism MH - Male MH - Monocytes/drug effects/metabolism MH - Neutrophils/drug effects/metabolism MH - Ozone/administration & dosage/immunology/*toxicity MH - Phagocytes/*drug effects/immunology/metabolism MH - Respiratory System/*drug effects/*immunology MH - Sputum/cytology/immunology/metabolism MH - Tumor Necrosis Factor-alpha/metabolism MH - Young Adult PMC - PMC3162474 MID - NIHMS317879 EDAT- 2010/06/15 06:00 MHDA- 2010/10/14 06:00 PMCR- 2011/08/26 CRDT- 2010/06/15 06:00 PHST- 2010/06/15 06:00 [entrez] PHST- 2010/06/15 06:00 [pubmed] PHST- 2010/10/14 06:00 [medline] PHST- 2011/08/26 00:00 [pmc-release] AID - 10.3109/08958371003610966 [doi] PST - ppublish SO - Inhal Toxicol. 2010 Jul;22(8):648-56. doi: 10.3109/08958371003610966.