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Comparative airway inflammatory response of normal volunteers to ozone and lipopolysaccharide challenge
Citation:
Hernandez, M. L., B. Harris, J. C. Lay, P. A. Bromberg, R. B. DEVLIN, S. R. Kleeberger, N. E. Alexis, AND D. B. Peden. Comparative airway inflammatory response of normal volunteers to ozone and lipopolysaccharide challenge. INHALATION TOXICOLOGY. Informa Healthcare USA, New York, NY, 22(8):648-56, (2010).
Impact/Purpose:
Ozone and LPS exposure in healthy volunteers induce simiiar neutrophil responses in the airways; however, downstream activation of innate immune responses differ, suggesting that oxidant versus bacterial air pollutants maybe mediated by different mechanisms.
Description:
Ozone and lipopolysaccharide (LPS) are environmental pollutants with adverse heatth 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 2h while performing Intermittent moderate exerclse,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 superatants were assayed for cytokine concentration. Both ozone and LPS challenge augmented sputum neutrophils and subject's 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. Howeverr 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 simiiar neutrophil responses in the airways; however, downstream activation of innate immune responses differ, suggesting that oxidant versus bacterial air pollutants maybe mediated by different mechanisms.
