Differences in airway reactivity in normal and allergic sheep after exposure to sulfur dioxide

Abraham, William M.; Oliver, William J.; Welker, Matthew; King, M.; Wanner, Adam; Sackner, Marvin A.

doi:10.1152/jappl.1981.51.6.1651

Cited by 14 publications

(4 citation statements)

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“…noted that in healthy non‐smokers, MCC significantly accelerated after 2.5 hours of exposure to sulfur dioxide, which was caused by an increase in ciliary beat frequency. However, excessive sulfur dioxide caused a decrease in MCC . Like phytohormones, the effect of sulfur dioxide on cilia is dependent on the concentration; low concentration causes promotion and high concentration causes inhibition.…”

Section: Environmental Pollutantsmentioning

confidence: 99%

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Environmental pollutants damage airway epithelial cell cilia: Implications for the prevention of obstructive lung diseases

et al. 2020

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Mucociliary epithelium lining the upper and lower respiratory tract constitutes the first line of defense of the airway and lungs against inhaled pollutants and pathogens. The concerted beating of multiciliated cells drives mucociliary clearance. Abnormalities in both the structure and function of airway cilia have been implicated in obstructive lung diseases. Emerging evidence reveals a close correlation between lung diseases and environmental stimuli such as sulfur dioxide and tobacco particles. However, the underlying mechanism remains to be described. In this review, we emphasize the importance of airway cilia in mucociliary clearance and discuss how environmental pollutants affect the structure and function of airway cilia, thus shedding light on the function of airway cilia in preventing obstructive lung diseases and revealing the negative effects of environmental pollutants on human health.

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Section: Environmental Pollutantsmentioning

confidence: 99%

“…However, excessive sulfur dioxide caused a decrease in MCC. 46 Like phytohormones, the effect of sulfur dioxide on cilia is dependent on the concentration; low concentration causes promotion and high concentration causes inhibition.…”

Section: Sulfur Dioxidementioning

confidence: 99%

Environmental pollutants damage airway epithelial cell cilia: Implications for the prevention of obstructive lung diseases

et al. 2020

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“…This model shares many characteristics of the disease in humans, including the development of early airway responses (EAR) and late airway responses (LAR) and postantigen-induced airway hyper-responsiveness (AHR) after inhalation challenge with Ascaris suum antigen (Abraham 2000). The model also demonstrates nonspecific bronchial hyperresponsiveness to a variety of agents, and we have previously used it to study the pulmonary consequences of pollutant exposures (Abraham et al 1980, 1981). Furthermore, the antigen-induced effects in this model can be ameliorated with the current armamentarium of clinically available asthma medications, including glucocorticosteroids, β 2 adrenergic agents, and leukotriene antagonists (Abraham 2000).…”

mentioning

confidence: 99%

Effects of Inhaled Brevetoxins in Allergic Airways: Toxin–Allergen Interactions and Pharmacologic Intervention

Abraham

Bourdelais

Ahmed

et al. 2005

Environ Health Perspect

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During a Florida red tide, brevetoxins produced by the dinoflagellate Karenia brevis become aerosolized and cause airway symptoms in humans, especially in those with pre-existing airway disease (e.g., asthma). To understand these toxin-induced airway effects, we used sheep with airway hypersensitivity to Ascaris suum antigen as a surrogate for asthmatic patients and studied changes in pulmonary airflow resistance (RL) after inhalation challenge with lysed cultures of K. brevis (crude brevetoxins). Studies were done without and with clinically available drugs to determine which might prevent/reverse these effects. Crude brevetoxins (20 breaths at 100 pg/mL; n = 5) increased R L 128 ± 6% (mean ± SE) over baseline. This bronchoconstriction was significantly reduced (% inhibition) after pretreatment with the glucocorticosteroid budesonide (49%), the β 2 adrenergic agent albuterol (71%), the anticholinergic agent atropine (58%), and the histamine H1-antagonist diphenhydramine (47%). The protection afforded by atropine and diphenhydramine suggests that both cholinergic (vagal) and H1-mediated pathways contribute to the bronchoconstriction. The response to cutaneous toxin injection was also histamine mediated. Thus, the airway and skin data support the hypothesis that toxin activates mast cells in vivo. Albuterol given immediately after toxin challenge rapidly reversed the bronchoconstriction. Toxin inhalation increased airway kinins, and the response to inhaled toxin was enhanced after allergen challenge. Both factors could contribute to the increased sensitivity of asthmatic patients to toxin exposure. We conclude that K. brevis aerosols are potent airway constrictors. Clinically available drugs may be used to prevent or provide therapeutic relief for affected individuals.

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“…It has been demonstrated that AHR can be induced by inhaled carbachol, histamine [190] or by methacholin [191] in challenged sheep. Pulmonary hyperreactivity can also be produced in sheep by inhalation of noxious substances, such as sulphur dioxide [192].…”

Section: Airway Hyperreactivitymentioning

confidence: 99%

Current Animal Models of Bronchial Asthma

Kurucz¹,

Szelenyi²

2006

CPD

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Human asthma is on the rise worldwide. The necessity to develop effective treatments against it requires an organized effort which covers every aspect of the disease from the pathological alterations via the genetic background to the use and development of active remedies. In these processes animal experiments have served an indispensable role. As asthma is not a natural disease in the animal kingdom the variety for artificially established animal models is quite wide. The possible selection ranges from the laboratory mouse to the horse, it includes ferret and sheep and even favorite pets such as cats and dogs. The large number of the models indicates that to some extent they might not be appropriate or it means that there is no generally accepted model of human asthma. Whatever the reason for this diversity animal models helped us to understand the detailed pathogenesis of some aspects of the disease, they helped us to develop compounds which are more active then previously used ones, and these models proved to us that human asthma is a unique, possibly species-specific disease the eradication of which requires a huge effort. This enormous task should include the collaboration of the clinical and basic research for the development of improved, advanced animal models, which in turn could strengthen our understanding about human asthma.

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Differences in airway reactivity in normal and allergic sheep after exposure to sulfur dioxide

Cited by 14 publications

References 0 publications

Environmental pollutants damage airway epithelial cell cilia: Implications for the prevention of obstructive lung diseases

Environmental pollutants damage airway epithelial cell cilia: Implications for the prevention of obstructive lung diseases

Effects of Inhaled Brevetoxins in Allergic Airways: Toxin–Allergen Interactions and Pharmacologic Intervention

Current Animal Models of Bronchial Asthma

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