Respiratory research, 2012-10, Vol.13 (1), p.89-89, Article 89
2012
Details
- Autor(en) / Beteiligte
- Titel
- Individuals with increased inflammatory response to ozone demonstrate muted signaling of immune cell trafficking pathways
- Ist Teil von
- Respiratory research, 2012-10, Vol.13 (1), p.89-89, Article 89
- Ort / Verlag
- England: BioMed Central Ltd
- Erscheinungsjahr
- 2012
- Link zum Volltext
- Quelle
- EZB-FREE-00999 freely available EZB journals
- Beschreibungen/Notizen
- 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. Determine baseline predictors and post exposure discriminators for the immuno-inflammatory response to ozone in inflammatory responsive adult volunteers. 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. 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. 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1465-993X, 1465-9921eISSN: 1465-993XDOI: 10.1186/1465-9921-13-89Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3607990
- Format
- –
- Schlagworte
- Adult, Air Pollutants - adverse effects, Air pollution, Allergies, Asthma - chemically induced, Asthma - genetics, Asthma - immunology, Biology, Biomarkers - metabolism, Cell Movement - drug effects, Cytokines, Cytokines - metabolism, Endorsements, Environmental health, Environmental protection, Fc receptors, Female, Gene expression, Gene Expression Profiling, Genetic Predisposition to Disease, Genotype & phenotype, Health care, Humans, Hypersensitivity, Immediate - chemically induced, Hypersensitivity, Immediate - genetics, Hypersensitivity, Immediate - immunology, Immune response, Immune system, Immunity, Innate - drug effects, Inflammation, Inflammation - chemically induced, Inflammation - genetics, Inflammation - immunology, Inflammation Mediators - metabolism, Inhalation Exposure - adverse effects, Lung - drug effects, Lung - immunology, Macrophages - drug effects, Macrophages - immunology, Male, Medicine, Neutrophils - drug effects, Neutrophils - immunology, Outdoor air quality, Ozone, Ozone - adverse effects, Phagocytosis - drug effects, Phenotype, Public health, Respiratory Burst - drug effects, Respiratory diseases, Rodents, Signal Transduction - drug effects, Sputum - immunology, Studies, Systems Biology, Time Factors, Transcription, Genetic - drug effects, Young Adult