title: Enhanced acute responses in an experimental exposure model to biomass smoke inhalation in chronic obstructive pulmonary disease.
abstract: Chronic obstructive pulmonary diseases (COPD) may increase air pollution-related mortality. The relationship of immune mechanisms to mortality caused by fine particulates in healthy and COPD populations is incompletely understood. The objective of this study was to determine whether fine particulates from a single biomass fuel alter stress and inflammation biomarkers in people with COPD. Healthy and COPD subjects were exposed to smoke in a controlled indoor setting. Immune responses were quantified by measuring cell surface marker expression with flow-cytometric analysis and mRNA levels with quantitative reverse transcriptase-polymerase chain reactions in whole blood before and after exposure. Preexposure COPD subjects had more leukocytes, mainly CD14(+) monocytes and neutrophils, but fewer CD3(+) T cells. Fifty-seven of 186 genes were differentially expressed between healthy and COPD subjects' peripheral blood mononuclear cells (PBMCs). Of these, only nuclear factor (NF)-kappa B1, TIMP-1, TIMP-2, and Duffy genes were up-regulated in COPD subjects. At 4 hours post smoke exposure, monocyte levels decreased only in healthy subjects. Fifteen genes, particular to inflammation, immune response, and cell-to-cell signaling, were differentially expressed in COPD subjects, versus 4 genes in healthy subjects. The authors observed significant differences in subjects' PBMCs, which may elucidate the adverse effects of air pollution particulates on people with COPD.
authors.affiliation: Department of Experimental Pathology and Pharmacology, Schering-Plough Biopharma, Palo Alto, California, USA.
authors.forename: Jeanine D
authors.initials: JD
authors.lastname: Mattson
authors.forename: Brian M
authors.initials: BM
authors.lastname: Haus
authors.forename: Bela
authors.initials: B
authors.lastname: Desai
authors.forename: Wayne
authors.initials: W
authors.lastname: Ott
authors.forename: Beth
authors.initials: B
authors.lastname: Basham
authors.forename: Madhuri
authors.initials: M
authors.lastname: Agrawal
authors.forename: Wei
authors.initials: W
authors.lastname: Ding
authors.forename: Lynn M
authors.initials: LM
authors.lastname: Hildemann
authors.forename: Karin M
authors.initials: KM
authors.lastname: Abitorabi
authors.forename: James
authors.initials: J
authors.lastname: Canfield
authors.forename: Gordon
authors.initials: G
authors.lastname: Mak
authors.forename: Sebnem
authors.initials: S
authors.lastname: Guvenc-Tuncturk
authors.forename: Rene de Waal
authors.initials: Rde W
authors.lastname: Malefyt
authors.forename: Terrill K
authors.initials: TK
authors.lastname: McClanahan
authors.forename: Robert B
authors.initials: RB
authors.lastname: Fick
authors.forename: Ware G
authors.initials: WG
authors.lastname: Kuschner
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers; D018533:Biomass; D002318:Cardiovascular Diseases / Q000209:etiology; D005434:Flow Cytometry; D020869:Gene Expression Profiling; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D016130:Immunophenotyping; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D008875:Middle Aged; D052638:Particulate Matter / Q000009:adverse effects*; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012906:Smoke / Q000009:adverse effects*
chemical_list: D015415:Biomarkers; D006684:HLA-DR Antigens; D018950:Lipopolysaccharide Receptors; D052638:Particulate Matter; D012906:Smoke