Mechanisms contributing to ozone-induced bronchial hyperreactivity in guinea-pigs

Yeadon, Michael; Wilkinson, Doris; Darley‐Usmar, Victor; O'leary, Vanessa J.; Payne, A.N.

doi:10.1016/0952-0600(92)90016-a

Cited by 41 publications

(22 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A further different mechanism might be responsible for the O 3 -induced airway hyperresponsiveness to substance P: a reduced activity of the neutral endopeptidase, the enzyme which cleaves substance P in addition to other tachykinins [47,63]. Indeed, neutral endopeptidase activity in tracheal tissue homogenate is significantly reduced in the guinea-pig by 2 h of exposure to 3 ppm O 2 [53].…”

Section: Effects Of Lung Function and Airway Responsivenessmentioning

confidence: 99%

Effect of oxidant air pollutants on the respiratory system: insights from experimental animal research

Chitano¹,

Hosselet²,

Mapp³

et al. 1995

Eur Respir J

100

View full text Add to dashboard Cite

In the present paper, we have reviewed experimental animal studies on the effects of the two most important oxidant airborne pollutants, nitrogen dioxide and ozone, on the respiratory system.The toxic effects depend on concentration and length of exposure, and are generally similar for both oxidants, with ozone operative at lower concentrations. High doses of both oxidants cause death due to lung oedema Exposure to sublethal levels causes functional alterations such as airflow limitation and airway hyperresponsiveness to bronchoconstrictor stimuli. These effects, which are generally reversible, are associated with epithelial injury, oedema and airway and parenchymal infiltration by inflammatory cells. Loss of cilia of airway epithelium and necrosis of type I alveolar epithelial cells are the most prominent consequences at the epithelial level. Inmation is characterized by early neutrophilic infiltration, followed by an increased number of mononuclear cells, predominantly alveolar macrophages.After long-term exposure, whilst nitrogen dioxide causes predominantly emphysema, ozone produces mainly pulmonary fibrosis. Biochemical effects include lipid peroxidation, increased antioxidant metabolism, and alteration of enzyme activity. Nitrogen dioxide and ozone may also alter the immunological response and reduce the defence against infections, increasing the susceptibility of exposed animals to infections.

show abstract

Section: Effects Of Lung Function and Airway Responsivenessmentioning

confidence: 99%

Effect of oxidant air pollutants on the respiratory system: insights from experimental animal research

Chitano¹,

Hosselet²,

Mapp³

et al. 1995

Eur Respir J

100

View full text Add to dashboard Cite

show abstract

“…In exposure chamber studies, use has been made of a metered gas delivery system [27], analytical chemical methods [11,[28][29][30], gas adsorbent tubes [31,32] and gas analysers [33][34][35], or other gas sensors providing a continuous read-out. Our choice of gas sensor was influenced by three factors, namely reliability, sensitivity and cost.…”

Section: Discussionmentioning

confidence: 99%

A method for the long-term exposure of rabbits to environmental pollutant gases

Douglas

Price²,

Page³

1994

Eur Respir J

View full text Add to dashboard Cite

A A m me et th ho od d f fo or r t th he e l lo on ng g--t te er rm m e ex xp po os su ur re e o of f r ra ab bb bi it ts s t to o e en nv vi ir ro on nm me en nt ta al l p po ol ll lu ut ta an nt t g ga as se es s ABSTRACT: The aims of the present study were twofold. Firstly, we wanted to develop a system for the exposure of rabbits to pollutant gases that would monitor gas concentrations accurately, allow flexibility, be simple to operate, and could be constructed at relatively modest cost. Additionally, we wanted to determine whether the procedures necessary for the daily exposure of young rabbits had any detrimental effect on their development. Using the environmental exposure system that we developed, littermate New Zealand White rabbits, neonatally immunized to either Alternaria tenuis or house dust mite antigen were exposed 2 h daily, from within 24 h of birth until 3 months of age, to either 4 ppm nitrogen dioxide (NO 2 ), or 5 ppm sulphur dioxide (SO 2 ) or ambient air.The environmental exposure system consists of four sections; a stainless steel exposure chamber; an airflow monitoring and control system and gas delivery system; a gas detector and monitoring system; and an exhaust fan. Equilibration and wash-out times of gas were short and the gas mixing within the chamber atmosphere was uniform. Levels of gases were reliably maintained throughout the period of exposure within predetermined limits. The weights of the immunized, gas-exposed animals did not differ significantly from those of the immunized, airexposed animals at any time throughout the 3 month period of exposure. At 3 months of age, the basal values for lung resistance and dynamic compliance did not differ between gas-and air-exposed rabbits. These values did not differ significantly from those obtained from naive animals of the same age.Our results suggest that we have developed a sensitive, reliable and simple environmental exposure and monitoring system. It is anticipated that the methodology described will allow the careful investigation of the effects of long-term exposure to pollutant gases from birth on the development of airways hyperresponsiveness.

show abstract

“…The in¯ammation and airway hyper-responsiveness associated with a variety of air pollutants are reduced in animals whose sensory ®bers have been destroyed by capsaicin-treatments or interrupted with antagonists to neuropeptide or capsaicin receptors (Prior et al, 1990;Nielsen, 1991;Yeadon et al, 1992;Satoh et al, 1993;Scheerens et al, 1996). The relevance of sensory innervation and its irritant receptors to ROFA in¯ammation was subsequently examined in a murine model of airway hyper-responsiveness.…”

Section: Role Of Vr1 Receptors In Rofa Inflammationmentioning

confidence: 99%

“…The sensory nervous system and NGI is associated with the chronic in¯ammation and airway remodeling reported in asthmatics (Barnes, 1999;Holt et al, 1999) and that associated with respiratory irritants such as ozone (Gordon et al, 1985;Yeadon et al, 1992;Joad et al, 1996;Albright and Goldstein, 1996), sulfur dioxide (Koenig andPierson, 1991) (el-Fawal et al, 1995), hydrogen sul®de (Prior et al, 1990), acrolein (Springall et al, 1990) and toluene diisocyanate (Sheppard and Scypinski, 1988;Gagnaire et al, 1997). Disease states such as asthma or viral infections are often marked by damage to the epithelial cell population which lines the nasal and pulmonary lumen.…”

Section: Neurogenic Inflammation and Environmentallyrelevant Airway Dmentioning

confidence: 99%

Neurogenic Inflammation and Particulate Matter (PM) Air Pollutants

Veronesi

Oortgiesen

2001

NeuroToxicology

View full text Add to dashboard Cite

Exposure to a class of airborne pollutants known as particulate matter (PM) is an environmental health risk of global proportions. PM is thought to initiate and/or exacerbate respiratory disorders, such as asthma and airway hyperresponsiveness and is epidemiologically associated with causing death in the elderly and those with pre-existing respiratory or cardiopulmonary disease. Plausible mechanisms of action to explain PM in¯ammation and its susceptible sub-population component are lacking. This review describes a series of published studies which indicate that PM initiates airway in¯ammation through sensory neural pathways, speci®cally by activation of capsaicin-sensitive vanilloid (e.g. VR1) irritant receptors. These acid-sensitive receptors are located on the sensory C nerve ®bers that innervate the airways as well as on various immune and non-immune airway target cells. The activation of these receptors results in the release of neuropeptides from the sensory terminals that innervate the airways. Their interactions with airway target cells, result in signs of in¯ammation (e.g. bronchoconstriction, vasodilation, histamine release, mucous secretion etc.). Our data have linked the activation of the VR1 receptors to the surface charge carried on the colloidal particulates which constitute PM pollution. Related studies have examined how genetic and non-genetic factors modify the sensitivity of these irritant receptors and enhance the in¯ammatory responsiveness to PM. In summary, this review proposes a mechanism by which neurogenic elements initiate and sustain PM-mediated airway in¯ammation. Although neurogenic in¯uences have been appreciated in normal airway homeostasis, they have not, until now, been associated with PM toxicity. The sensitivity of the sensory nervous system to irritants and its interactions with pulmonary target tissues, should encourage neuroscientists to explore the relevance of neurogenic in¯uences to toxic disorders involving other peripheral target systems. Crown

show abstract

Mechanisms contributing to ozone-induced bronchial hyperreactivity in guinea-pigs

Cited by 41 publications

References 38 publications

Effect of oxidant air pollutants on the respiratory system: insights from experimental animal research

Effect of oxidant air pollutants on the respiratory system: insights from experimental animal research

A method for the long-term exposure of rabbits to environmental pollutant gases

Neurogenic Inflammation and Particulate Matter (PM) Air Pollutants

Contact Info

Product

Resources

About