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Open Access Research

Individuals with increased inflammatory response to ozone demonstrate muted signaling of immune cell trafficking pathways

Rebecca C Fry1, Julia E Rager1, Haibo Zhou23, Baiming Zou3, June W Brickey4, Jenny Ting4, John C Lay25, David B Peden25 and Neil E Alexis25*

Author Affiliations

1 Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA

2 Center for Environmental Medicine, Asthma, and Lung Biology, School of Medicine, University of North Carolina, Chapel Hill, NC, USA

3 Biostatistics, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA

4 Department of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

5 Department of Pediatrics, University of North Carolina, School of Medicine University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

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Respiratory Research 2012, 13:89  doi:10.1186/1465-9921-13-89

Published: 3 October 2012

Abstract

Background

Exposure to ozone activates innate immune function and causes neutrophilic (PMN) airway inflammation that in some individuals is robustly elevated. The interplay between immuno-inflammatory function and genomic signaling in those with heightened inflammatory responsiveness to ozone is not well understood.

Objectives

Determine baseline predictors and post exposure discriminators for the immuno-inflammatory response to ozone in inflammatory responsive adult volunteers.

Methods

Sputum induction was performed on 27 individuals before and after a two hour chamber exposure to 0.4 ppm ozone. Subjects were classified as inflammatory responders or non-responders to ozone based on their PMN response. Innate immune function, inflammatory cell and cytokine modulation and transcriptional signaling pathways were measured in sputum.

Results

Post exposure, responders showed activated innate immune function (CD16: 31,004 MFI vs 8988 MFI; CD11b: 44,986 MFI vs 24,770 MFI; CD80: 2236 MFI vs 1506 MFI; IL-8: 37,603 pg/ml vs 2828 pg/ml; and IL-1β: 1380 pg/ml vs 318 pg/ml) with muted signaling of immune cell trafficking pathways. In contrast, non-responders displayed decreased innate immune activity (CD16, CD80; phagocytosis: 2 particles/PMN vs 4 particles/PMN) post exposure that was accompanied by a heightened signaling of immune cell trafficking pathways.

Conclusions

Inflammatory responsive and non responsive individuals to ozone show an inverse relationship between immune cell trafficking and immuno-inflammatory functional responses to ozone. These distinct genomic signatures may further our understanding about ozone-induced morbidity in individuals with different levels of inflammatory responsiveness.

Keywords:
Air pollution; Environment; Ozone; Gene expression; Human sputum; Immune response; Innate immunity; Systems biology