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)-κ 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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 631-662 |
| Number of pages | 32 |
| Journal | Experimental Lung Research |
| Volume | 34 |
| Issue number | 10 |
| DOIs | |
| State | Published - Dec 2008 |
| Externally published | Yes |
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Keywords
- Chronic obstructive
- Flow cytometric analysis
- Forced expiratory flow
- Forced expiratory volume
- Forced vital capacity
- Pulmonary disease
- Reverse transcriptase-polymerase chain reaction
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Molecular Biology
- Clinical Biochemistry
Cite this
Enhanced acute responses in an experimental exposure model to biomass smoke inhalation in chronic obstructive pulmonary disease. / Mattson, Jeanine D.; Haus, Brian; Desai, Bela; Ott, Wayne; Basham, Beth; Agrawal, Madhuri; Ding, Wei; Hildemann, Lynn M.; Abitorabi, Karin M.; Canfield, James; Mak, Gordon; Guvenc-Tuncturk, Sebnem; Malefyt, Rene De Waal; McClanahan, Terrill K.; Fick, Robert B.; Kuschner, Ware G.
In: Experimental Lung Research, Vol. 34, No. 10, 12.2008, p. 631-662.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Enhanced acute responses in an experimental exposure model to biomass smoke inhalation in chronic obstructive pulmonary disease
AU - Mattson, Jeanine D.
AU - Haus, Brian
AU - Desai, Bela
AU - Ott, Wayne
AU - Basham, Beth
AU - Agrawal, Madhuri
AU - Ding, Wei
AU - Hildemann, Lynn M.
AU - Abitorabi, Karin M.
AU - Canfield, James
AU - Mak, Gordon
AU - Guvenc-Tuncturk, Sebnem
AU - Malefyt, Rene De Waal
AU - McClanahan, Terrill K.
AU - Fick, Robert B.
AU - Kuschner, Ware G.
PY - 2008/12
Y1 - 2008/12
N2 - 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)-κ 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.
AB - 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)-κ 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.
KW - Chronic obstructive
KW - Flow cytometric analysis
KW - Forced expiratory flow
KW - Forced expiratory volume
KW - Forced vital capacity
KW - Pulmonary disease
KW - Reverse transcriptase-polymerase chain reaction
UR - http://www.scopus.com/inward/record.url?scp=57749107491&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=57749107491&partnerID=8YFLogxK
U2 - 10.1080/01902140802322256
DO - 10.1080/01902140802322256
M3 - Article
C2 - 19085563
AN - SCOPUS:57749107491
VL - 34
SP - 631
EP - 662
JO - Experimental Lung Research
JF - Experimental Lung Research
SN - 0190-2148
IS - 10
ER -