Comparative sensitivity of measurements of lung damage made by bronchoalveolar lavage after short-term exposure of rats to ozone

Guth, Daniel J.; Warren, Darren L.

doi:10.1016/0300-483x(86)90074-0

Cited by 68 publications

(27 citation statements)

References 27 publications

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“…In addition to age, qualitative difference in nonimmunologic responses to 03 among animal species have also been documented (121)(122)(123)(124)(125)(126)(127). Also, it is becoming increasingly clear that pulmonary responses to 0 exposure is subject to genetic infuence (128)(129)(130)(131)(132), and it is also known that the immune response is under genetic control (133,134 (Figure 11).…”

Section: Considerations Ofhost Factorsmentioning

confidence: 98%

The Effects of Ozone on Immune Function

Jakab¹,

Spannhake²,

Canning³

et al. 1995

Environmental Health Perspectives

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A review of the literature reveals that ozone (03) exposure can either suppress or enhance immune responsiveness. These disparate effects elicited by 0 exposure depend, in large part, on the experimental design used, the immune parameters examined as well as the animal species studied.Despite the apparent contradictions, a general pattern of response to 03 exposure can be recognized. Most studies indicate that continuous 03 exposure leads to an early (days 0-3) impairment of immune responsiveness followed, with continued exposures, by a form of adaptation to 03 that results in a re-establishment of the immune response. The effects of 03 exposure on the response to antigenic stimulation also depend on the time at which 03 exposure occurred. Whereas 03 exposure prior to immunization is without effect on the response to antigen, 03 exposure subsequent to immunization suppresses the response to antigen. Although most studies have focused on immune responses in the lung, numerous investigators have provided functional and anatomical evidence to support the hypothesis that 03 exposure can have profound effects on systemic immunity. -Environ Health Perspect 1 03(Suppl 2): 77-89 (1995)

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Section: Considerations Ofhost Factorsmentioning

confidence: 98%

The Effects of Ozone on Immune Function

Jakab¹,

Spannhake²,

Canning³

et al. 1995

Environmental Health Perspectives

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“…A macroscopic consequence of oedema formation after exposure to these two oxidants consists of increased lung volume and wet weight [32,76,77,81]. A sensitive index of lung oedema, which constitutes a common finding after exposure both to NO 2 and O 3 , is the presence of serum proteins in the bronchoalveolar lavage fluid [82][83][84][85]. Alteration of epithelial and vascular permeability leading to oedema is particularly marked at small airway and alveolar levels [75,[85][86][87][88].…”

Section: Histopathologymentioning

confidence: 99%

“…Tracheal permeability develops immediately after exposure to oxidant gases [83][84][85][86][87][88][103][104][105][106] and reaches a peak at 8 h postexposure, whilst the number of polymorphonuclear leucocytes usually peaks at 12 h [103]. Rats rendered leukopenic with cyclophosphamide have a significant reduction in circulating and pulmonary leucocytes and in airway permeability induced by O 3 , and pretreatment with either the LTD 4 antagonist FPL55712 or indomethacin also inhibits the O 3 -induced increase in permeability [104].…”

Section: Histopathologymentioning

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

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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.

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“…Calibration was checked against an absolute ozone monitor (Dasibi Model 1008-PC). The three-day interval was chosen to maximize the inflammatory response (Guth et al, 1986). This protocol gives the same (or greater) response as exposure to the same total dose of ozone for 24 hours (Gelzleichter et al, 1992).…”

Section: Exposure To Ozonementioning

confidence: 99%

Differentiation of the roles of NO from airway epithelium and inflammatory cells in ozone-induced lung inflammation

Kenyon

Eiserich

Morrissey

et al. 2006

Toxicology and Applied Pharmacology

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Mice lacking inducible nitric oxide synthase (NOS2−/−) are more susceptible to ozone-induced lung inflammation and injury than their isogenic wild-type (NOS2+/+) counterparts, demonstrating an apparent protective effect for NOS2 in murine lungs. We hypothesized that nitric oxide (NO) generated from either NOS2 in the airway epithelial cells or the bone marrow-derived inflammatory cells was responsible for the protective effect of NOS2. To test this hypothesis, we prepared chimeric mice by killing their endogenous bone marrow cells by whole body irradiation, followed by bone marrow transplantation from a heterologous donor mouse. We exposed C57BL/6 (NOS2+/+), NOS2 −/−, and chimeric NOS2 mice (NOS2−/+, NOS2+/−) to 1 ppm of ozone for 3 consecutive nights. NOS2−/− mice were more severely injured after exposure to ozone than C57BL/6 mice, including a more robust inflammatory cell influx (4.14×10 5 ±2.19×10 5 vs. 2.78 ×10 5 ± 1.36×10 5 cells respectively; p=0.036) and greater oxidation of total protein sulfhydryls (R-SH) in their blood plasma. Chimeric NOS2 −/+ mice, which had bone marrow from NOS2−/− mice transplanted into C57BL/ 6 recipients, had a significantly greater response to ozone (increased numbers of neutrophils in lung lavage and decreased concentrations of exhaled NO) as compared to the reciprocal chimeric strain (NOS2+/−). We conclude that NOS2 has a protective effect against acute lung injury caused by ozone inhalation, which may be mediated, in part, by NO generated by NOS2 from inflammatory cells, predominantly neutrophils, recruited into the lung.

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Comparative sensitivity of measurements of lung damage made by bronchoalveolar lavage after short-term exposure of rats to ozone

Cited by 68 publications

References 27 publications

The Effects of Ozone on Immune Function

The Effects of Ozone on Immune Function

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

Differentiation of the roles of NO from airway epithelium and inflammatory cells in ozone-induced lung inflammation

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