Cell vs. Noncell Airway Temporal Response in Rats Exposed to Sulfur Dioxide

Knauss, Harold J.; Robinson, William E.; Tc, Medici; Chodosh, Sanford

doi:10.1080/00039896.1976.10667227

Cited by 4 publications

(3 citation statements)

References 16 publications

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“…SO 2 -induced bronchitis in the rat has been considered a model of chronic human bronchitis because mucus hypersecretion and chronic mucus cell metaplasia are persistent and progressively increased during the course of SO 2 exposure (Farone et al, 1995;Knauss et al, 1976). The concentrations of SO 2 used for developing bronchitis range from 200 to 600 ppm, depending on animal species and strain.…”

Section: Discussionmentioning

confidence: 99%

Variable Pulmonary Responses from Exposure to Concentrated Ambient Air Particles in a Rat Model of Bronchitis

Kodavanti

Mebane²,

Ledbetter³

et al. 2000

Toxicological Sciences

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Chronic bronchitis may be considered a risk factor in particulate matter (PM)-induced morbidity. We hypothesized that a rat model of human bronchitis would be more susceptible to the pulmonary effects of concentrated ambient particles (CAPs) from Research Triangle Park, NC. Bronchitis was induced in male Sprague-Dawley rats (90-100 days of age) by exposure to 200 ppm sulfur dioxide (SO2), 6 h/day x 5 days/week x 6 weeks. One day following the last SO2 exposure, both healthy (air-exposed) and bronchitic (SO2-exposed) rats were exposed to filtered air (three healthy; four bronchitic) or CAPs (five healthy; four bronchitic) by whole-body inhalation, 6 h/day x 2 or 3 days. Pulmonary injury was determined either immediately (0h) or 18 h following final CAPs exposure. The study protocol involving 0 h time point was repeated four times (study #A, November, 1997; #B, February, 1998; #C and #D, May, 1998), whereas the study protocol involving 18 h time point was done only once (#F). In an additional study (#E), rats were exposed to residual oil fly ash (ROFA), approximately 1 mg/ m(3)x6 h/day x 3 days to mimic the CAPs protocol (February, 1998). The rats allowed 18 h recovery following CAPs exposure (#F) did not depict any CAPs-related differences in bronchoalveolar lavage fluid (BALF) injury markers. Of the four CAPs studies conducted (0 h time point), the first (#A) study (approximately 650 microg/m3 CAPs) revealed significant changes in the lungs of CAPs-exposed bronchitic rats compared to the clean air controls. These rats had increased BALF protein, albumin, N-acetyl glutaminidase (NAG) activity and neutrophils. The second (#B) study (approximately 475 microg/m3 CAPs) did not reveal any significant effects of CAPs on BALF parameters. Study protocols #C (approximately 869 microg/m3 CAPs) and #D (approximately 907 microg/m3 CAPs) revealed only moderate increases in the above mentioned BALF parameters in bronchitic rats exposed to CAPs. Pulmonary histologic evaluation of studies #A, #C, #D, and #F revealed marginally higher congestion and perivascular cellularity in CAPs-exposed bronchitic rats. Healthy and bronchitic rats exposed to ROFA (approximately 1 mg/m3) did not show significant pulmonary injury (#E). Analysis of leachable elemental components of CAPs revealed the presence of sulfur, zinc, manganese, and iron. There was an apparent lack of association between pulmonary injury and CAPs concentration, or its leachable sulfate or elemental content. In summary, real-time atmospheric PM may result in pulmonary injury, particularly in susceptible models. However, the variability observed in pulmonary responses to CAPs emphasizes the need to conduct repeated studies, perhaps in relation to the season, as composition of CAPs may vary. Additionally, potential variability in pathology of induced bronchitis or other lung disease may decrease the ability to distinguish toxic injury due to PM.

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Section: Discussionmentioning

confidence: 99%

Variable Pulmonary Responses from Exposure to Concentrated Ambient Air Particles in a Rat Model of Bronchitis

Kodavanti

Mebane²,

Ledbetter³

et al. 2000

Toxicological Sciences

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“…There are inflammatory cells in the airway lumen as well as the airway tissue of rats with SO 2 ‐induced bronchitis. For example, inflammatory cells are observed in mucus isolated from these rats and increase in number with increasing duration of exposure [44]. We have also observed increased numbers of neutrophils in nasal, airway, and bronchoalveolar lavage fluid of SO 2 ‐exposed rats [37].…”

Section: Animal Models Of Chronic Bronchitismentioning

confidence: 92%

“…[43] reported an elevation in mucous content in bronchoalveolar lavage fluid obtained from SO 2 ‐exposed rats, while Knauss et al . [44] reported that the amount of mucus recovered increased with increasing duration of exposure. Taken together, these data indicate that chronic exposure of rats to SO 2 induces airway mucous hypersecretion.…”

Section: Animal Models Of Chronic Bronchitismentioning

confidence: 99%

Animal models of asthma and chronic bronchitis

Drazen

Takebayashi

Long

et al. 1999

Clin Experimental Allergy

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Human asthma is characterized by three critical phenotypic traits: intermittent reversible airway obstruction, airway hyperresponsiveness and airway inflammation. In animal models of asthma, airway hyperresponsiveness is an important feature. This trait is characterized by an exaggerated bronchoconstrictor response that would have little physiological consequence in an otherwise unaffected or normal individual. In this article we explore two distinct facets of airway responsiveness. The first is the genetic basis for variations in airway responsiveness that occur in mice in the absence of any specific environmental manipulation. We demonstrate that standard genetic approaches can be successfully applied to the identification of regions of the mouse genome linked to the expression of airway hyperresponsiveness. The second topic addressed in this review is the change in airway responsiveness induced in rats by repeated exposure to sulphur dioxide gas. With daily exposure to high concentrations of sulphur dioxide gas, there is chronic injury and repair of epithelial cells. Over time, rats develop mucous hypersecretion, airway inflammation, increased airway resistance and airway hyperresponsiveness. This model has provided useful information on the mechanisms underlying the pathophysiological events that typify the chronic bronchitis in humans.

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Animal Models

Shore

2002

Asthma and COPD

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Cell vs. Noncell Airway Temporal Response in Rats Exposed to Sulfur Dioxide

Cited by 4 publications

References 16 publications

Variable Pulmonary Responses from Exposure to Concentrated Ambient Air Particles in a Rat Model of Bronchitis

Variable Pulmonary Responses from Exposure to Concentrated Ambient Air Particles in a Rat Model of Bronchitis

Animal models of asthma and chronic bronchitis

Animal Models

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