TY - JOUR
T1 - Exposure to 1 ppm ozone attenuates the immediate antigenic response of canine peripheral airways
AU - Kleeberger, Steven R.
AU - Kolbe, John
AU - Turner, Claudia
AU - Spannhake, Ernst W.
N1 - Funding Information:
This study was supported by NIH grant ES-03505; S.R. Kleeberger was supported by R23 HL-37061; J. Kolbe was supported in part by theMaurice andPhyllis Paykel Trust, New Zealand; and C. Turner was supported by NIH training grant HL-07534. The authors gratefully thank Mr. Terry Adams andMr. Matthew Kovalsky for their excellent technical assistance. Thanks also to Cindy Rogers and Christine Tucker for their valuable aid in preparing this manuscript. Requests for reprints should besent to Steven R.Kleeberger, Ph.D., Division of Environmental Physiology, Johns Hopkins University, 615 North Wolfe Street, Baltimore, MD21205.
Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 1989/11/1
Y1 - 1989/11/1
N2 - The effect of oxidant exposure on the immediate airway response to immunologic challenge is controversial. We investigated the response of canine peripheral airways to antigen aerosol, 1-3 h and 24 h after a 5-min exposure to 1 ppm ozone. In dogs that were natively sensitive to Ascaris suum antigen, resistance to flow through the collateral system (Rcs) was measured using the wedged bronchoscope technique. In eight dogs, four sublobar segments of each lung were wedged: Two were exposed to ozone for 5 min and two (control) received air with 5% C02. Ozone caused a mean (±SE) increase in Rcsof 75 ± 15%, which returned to baseline after 1-3 h. The increase in Rcselicited by subsequent administration of antigen aerosol (25 μl, 0.27 mg proteinlml) to the ozone-exposed segments (312.0 ± 70.6%) was attenuated by 22% compared to controls (398.9 ± 83.0%; p <.05). In another series of experiments (n = 5), segments were exposed to ozone or air and challenged with antigen 24 h laterand a significant attenuation (38%) of the antigen-induced increase in Rcs was detected compared to controls (178.5 ± 57.9 vs. 289.0 ± 62.2; p <.05). Cellular influx of polymorphonuclear leukocytes (PMNs) was not detected by bronchoalveolar lavage (BAL) 1-3 h after ozone, but was found after24 h (19.8 vs. 4.7%; p <.01). A significant increase in PMNs was detected in exposed subepithelial tissues 1-3 h after ozone compared to unexposed tissues. Tissue PMNs were not significantly different from unexposed tissues after 24 h, but a shift toward degranulation of mast cells was detected in ozone-exposed tissues at this time. These data suggest that the Rcsresponse to antigen is attenuated 1-3 h and 24 h after acute (5 min) exposure to 1 ppm ozone, and this effect occurs independently of PMNs in the airways.
AB - The effect of oxidant exposure on the immediate airway response to immunologic challenge is controversial. We investigated the response of canine peripheral airways to antigen aerosol, 1-3 h and 24 h after a 5-min exposure to 1 ppm ozone. In dogs that were natively sensitive to Ascaris suum antigen, resistance to flow through the collateral system (Rcs) was measured using the wedged bronchoscope technique. In eight dogs, four sublobar segments of each lung were wedged: Two were exposed to ozone for 5 min and two (control) received air with 5% C02. Ozone caused a mean (±SE) increase in Rcsof 75 ± 15%, which returned to baseline after 1-3 h. The increase in Rcselicited by subsequent administration of antigen aerosol (25 μl, 0.27 mg proteinlml) to the ozone-exposed segments (312.0 ± 70.6%) was attenuated by 22% compared to controls (398.9 ± 83.0%; p <.05). In another series of experiments (n = 5), segments were exposed to ozone or air and challenged with antigen 24 h laterand a significant attenuation (38%) of the antigen-induced increase in Rcs was detected compared to controls (178.5 ± 57.9 vs. 289.0 ± 62.2; p <.05). Cellular influx of polymorphonuclear leukocytes (PMNs) was not detected by bronchoalveolar lavage (BAL) 1-3 h after ozone, but was found after24 h (19.8 vs. 4.7%; p <.01). A significant increase in PMNs was detected in exposed subepithelial tissues 1-3 h after ozone compared to unexposed tissues. Tissue PMNs were not significantly different from unexposed tissues after 24 h, but a shift toward degranulation of mast cells was detected in ozone-exposed tissues at this time. These data suggest that the Rcsresponse to antigen is attenuated 1-3 h and 24 h after acute (5 min) exposure to 1 ppm ozone, and this effect occurs independently of PMNs in the airways.
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U2 - 10.1080/15287398909531354
DO - 10.1080/15287398909531354
M3 - Article
C2 - 2585539
AN - SCOPUS:0024396805
SN - 0098-4108
VL - 28
SP - 349
EP - 362
JO - Journal of Toxicology and Environmental Health
JF - Journal of Toxicology and Environmental Health
IS - 3
ER -