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Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.

We tested the hypothesis that exposure of healthy volunteers to concentrated ambient air particles (CAPS) between 0.1 and 2.5 microm in diameter is associated with modulation of human alveolar macrophage (AM) function, cytokine production, and immune phenotype in both blood and lung. Thirty-eight vo...

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Autores principales: Harder, S D, Soukup, J M, Ghio, A J, Devlin, R B, Becker, S
Formato: Texto
Lenguaje:English
Publicado: 2001
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240588/
https://www.ncbi.nlm.nih.gov/pubmed/11544170
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author Harder, S D
Soukup, J M
Ghio, A J
Devlin, R B
Becker, S
author_facet Harder, S D
Soukup, J M
Ghio, A J
Devlin, R B
Becker, S
author_sort Harder, S D
collection PubMed
description We tested the hypothesis that exposure of healthy volunteers to concentrated ambient air particles (CAPS) between 0.1 and 2.5 microm in diameter is associated with modulation of human alveolar macrophage (AM) function, cytokine production, and immune phenotype in both blood and lung. Thirty-eight volunteers were exposed to either filtered air or CAPS from the immediate environment of the U.S. Environmental Protection Agency human studies facility in Chapel Hill, North Carolina, USA. Particle concentrations in the chamber during the exposures ranged from 23.1 to 311.1 microg/m3. No symptoms were noted by volunteers after the exposure. Eighteen hours after exposure, analysis of cells obtained by bronchoalveolar lavage (BAL) showed a mild increase in neutrophils in both the bronchial (8.4 +/- 2%) and alveolar fractions (4.2 +/- 1.7%) in subjects exposed to the highest concentration of CAPS compared to neutrophils in the fluids of those exposed to filtered air (bronchial fraction 2.7 +/- 0.6%; alveolar fraction 0.8 +/- 0.3%). There was no change in the percentage of lymphocytes or AMs recovered in the lavage after inhalation of the highest particle levels (mean 207 microg/m3). There was also no change in the proportion of lymphocytes in the BAL expressing CD3, CD4, CD8, CD19, nor activation markers CD25 or CD69. Particle inhalation did not affect the expression of CD11b, CD64, CD16, CD14, CD71 on AM, nor was there an effect on phagocytosis or oxidant generation following stimulation with zymosan A. IL-6 and IL-8 levels detected by enzyme-linked immunoabsorbent assay in the BAL were unrelated to inhaled particle levels. The distribution of lymphocyte subsets in blood obtained 18 hr after exposure to CAPS did not differ from that found before exposure. We conclude that ambient air particles are capable of inducing a mild inflammation in the lower respiratory tract but have no effect on immune phenotype or macrophage function under the conditions tested.
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spelling pubmed-12405882005-11-08 Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects. Harder, S D Soukup, J M Ghio, A J Devlin, R B Becker, S Environ Health Perspect Research Article We tested the hypothesis that exposure of healthy volunteers to concentrated ambient air particles (CAPS) between 0.1 and 2.5 microm in diameter is associated with modulation of human alveolar macrophage (AM) function, cytokine production, and immune phenotype in both blood and lung. Thirty-eight volunteers were exposed to either filtered air or CAPS from the immediate environment of the U.S. Environmental Protection Agency human studies facility in Chapel Hill, North Carolina, USA. Particle concentrations in the chamber during the exposures ranged from 23.1 to 311.1 microg/m3. No symptoms were noted by volunteers after the exposure. Eighteen hours after exposure, analysis of cells obtained by bronchoalveolar lavage (BAL) showed a mild increase in neutrophils in both the bronchial (8.4 +/- 2%) and alveolar fractions (4.2 +/- 1.7%) in subjects exposed to the highest concentration of CAPS compared to neutrophils in the fluids of those exposed to filtered air (bronchial fraction 2.7 +/- 0.6%; alveolar fraction 0.8 +/- 0.3%). There was no change in the percentage of lymphocytes or AMs recovered in the lavage after inhalation of the highest particle levels (mean 207 microg/m3). There was also no change in the proportion of lymphocytes in the BAL expressing CD3, CD4, CD8, CD19, nor activation markers CD25 or CD69. Particle inhalation did not affect the expression of CD11b, CD64, CD16, CD14, CD71 on AM, nor was there an effect on phagocytosis or oxidant generation following stimulation with zymosan A. IL-6 and IL-8 levels detected by enzyme-linked immunoabsorbent assay in the BAL were unrelated to inhaled particle levels. The distribution of lymphocyte subsets in blood obtained 18 hr after exposure to CAPS did not differ from that found before exposure. We conclude that ambient air particles are capable of inducing a mild inflammation in the lower respiratory tract but have no effect on immune phenotype or macrophage function under the conditions tested. 2001-08 /pmc/articles/PMC1240588/ /pubmed/11544170 Text en
spellingShingle Research Article
Harder, S D
Soukup, J M
Ghio, A J
Devlin, R B
Becker, S
Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.
title Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.
title_full Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.
title_fullStr Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.
title_full_unstemmed Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.
title_short Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.
title_sort inhalation of pm2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240588/
https://www.ncbi.nlm.nih.gov/pubmed/11544170
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