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

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.

journal_name

Respir Res

journal_title

Respiratory research

authors

Fry RC,Rager JE,Zhou H,Zou B,Brickey JW,Ting J,Lay JC,Peden DB,Alexis NE

doi

10.1186/1465-9921-13-89

subject

Has Abstract

pub_date

2012-10-03 00:00:00

pages

89

eissn

1465-9921

issn

1465-993X

pii

1465-9921-13-89

journal_volume

13

pub_type

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