Ozone-induced inflammation and altered ventilation in genetically susceptible mice: a comparison of acute and subacute exposures

Clarke G. Tankersley; Steven R. Kleeberger

doi:10.1016/0378-4274(94)90039-6

Ozone-induced inflammation and altered ventilation in genetically susceptible mice: a comparison of acute and subacute exposures

Clarke G. Tankersley, Steven R. Kleeberger

Bloomberg School of Public Health

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

We have examined whether the effects of acute (2 ppm/3 h) and subacute (0.3 ppm/72 h) ozone (O₃) exposures on airways are mutually predictive. Inbred C57BL/6J (susceptible) and C3H/HeJ (resistant) mice are differentially responsive to inflammation induced by the 2 exposures. Breeding experiments and cosegregation analysis indicated that 2 separate genes control inflammatory responses: Inf (acute), Inf-2 (subacute). The genetic model was also used to examine the effects of both exposures on the magnitude and pattern of breathing. Results imply that mechanisms that control susceptibility to the 2 exposures are not the same, and that one response is not necessarily predictive of the other.

Original language	English (US)
Pages (from-to)	279-289
Number of pages	11
Journal	Toxicology Letters
Volume	72
Issue number	1-3
DOIs	https://doi.org/10.1016/0378-4274(94)90039-6
State	Published - Jun 1994

Keywords

Airways
Bronchoalveolar lavage
Control of breathing
Cosegregation analysis
Hypercapnia
Inbred mice

ASJC Scopus subject areas

Toxicology

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10.1016/0378-4274(94)90039-6

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title = "Ozone-induced inflammation and altered ventilation in genetically susceptible mice: a comparison of acute and subacute exposures",

abstract = "We have examined whether the effects of acute (2 ppm/3 h) and subacute (0.3 ppm/72 h) ozone (O3) exposures on airways are mutually predictive. Inbred C57BL/6J (susceptible) and C3H/HeJ (resistant) mice are differentially responsive to inflammation induced by the 2 exposures. Breeding experiments and cosegregation analysis indicated that 2 separate genes control inflammatory responses: Inf (acute), Inf-2 (subacute). The genetic model was also used to examine the effects of both exposures on the magnitude and pattern of breathing. Results imply that mechanisms that control susceptibility to the 2 exposures are not the same, and that one response is not necessarily predictive of the other.",

keywords = "Airways, Bronchoalveolar lavage, Control of breathing, Cosegregation analysis, Hypercapnia, Inbred mice",

author = "Tankersley, {Clarke G.} and Kleeberger, {Steven R.}",

note = "Funding Information: This studyw as supportedb y EnvironmentaPl rotectionA gencyG rant R-816557, Center for Indoor Air ResearchG rant 90-27,a nd National Instituteso f Health Grants ES 03505,E S 03819,a nd HL 07534.",

year = "1994",

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doi = "10.1016/0378-4274(94)90039-6",

language = "English (US)",

volume = "72",

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journal = "Toxicology Letters",

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T2 - a comparison of acute and subacute exposures

AU - Tankersley, Clarke G.

AU - Kleeberger, Steven R.

N1 - Funding Information: This studyw as supportedb y EnvironmentaPl rotectionA gencyG rant R-816557, Center for Indoor Air ResearchG rant 90-27,a nd National Instituteso f Health Grants ES 03505,E S 03819,a nd HL 07534.

PY - 1994/6

Y1 - 1994/6

N2 - We have examined whether the effects of acute (2 ppm/3 h) and subacute (0.3 ppm/72 h) ozone (O3) exposures on airways are mutually predictive. Inbred C57BL/6J (susceptible) and C3H/HeJ (resistant) mice are differentially responsive to inflammation induced by the 2 exposures. Breeding experiments and cosegregation analysis indicated that 2 separate genes control inflammatory responses: Inf (acute), Inf-2 (subacute). The genetic model was also used to examine the effects of both exposures on the magnitude and pattern of breathing. Results imply that mechanisms that control susceptibility to the 2 exposures are not the same, and that one response is not necessarily predictive of the other.

AB - We have examined whether the effects of acute (2 ppm/3 h) and subacute (0.3 ppm/72 h) ozone (O3) exposures on airways are mutually predictive. Inbred C57BL/6J (susceptible) and C3H/HeJ (resistant) mice are differentially responsive to inflammation induced by the 2 exposures. Breeding experiments and cosegregation analysis indicated that 2 separate genes control inflammatory responses: Inf (acute), Inf-2 (subacute). The genetic model was also used to examine the effects of both exposures on the magnitude and pattern of breathing. Results imply that mechanisms that control susceptibility to the 2 exposures are not the same, and that one response is not necessarily predictive of the other.

KW - Airways

KW - Bronchoalveolar lavage

KW - Control of breathing

KW - Cosegregation analysis

KW - Hypercapnia

KW - Inbred mice

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Ozone-induced inflammation and altered ventilation in genetically susceptible mice: a comparison of acute and subacute exposures

Abstract

Keywords

ASJC Scopus subject areas

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