Time course of permeability changes and PMN flux in rat trachea following O3 exposure

Young, C.; Bhalla, Deepak K.

doi:10.1016/0272-0590(92)90043-h

Cited by 16 publications

(2 citation statements)

References 18 publications

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“…The corresponding values for CC16 are approximately 100 mg/L and 15 pg/L, assuming a free exchange of the protein across the endothelium (7). For CC16, acute exposure to 03 (B) causes an increased permeability of the epithelial barrier to proteins (9,17), resulting in an increased leakage of plasma albumin in the airways and, in the opposite direction, of CC16 into the interstitium from which it is cleared by lymphatic drainage or directly in the blood across the endothelium. exercising subjects exposed on average to 0.07 ppm 0 during 2 hr.…”

Section: Discussionmentioning

confidence: 99%

Serum clara cell protein: a sensitive biomarker of increased lung epithelium permeability caused by ambient ozone.

Broeckaert

Arsalane²,

Hermans³

et al. 2000

Environ Health Perspect

108

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Ozone in ambient air may cause various effects on human health, including decreased lung function, asthma exacerbation, and even premature mortality. These effects have been evidenced using various clinical indicators that, although sensitive, do not specifically evaluate the O(3)-increased lung epithelium permeability. In the present study, we assessed the acute effects of ambient O(3) on the pulmonary epithelium by a new approach relying on the assay in serum of the lung-specific Clara cell protein (CC16 or CC10). We applied this test to cyclists who exercised for 2 hr during episodes of photochemical smog and found that O(3) induces an early leakage of lung Clara cell protein. The protein levels increased significantly into the serum from exposure levels as low as 0.060-0.084 ppm. Our findings, confirmed in mice exposed to the current U.S. National Ambient Air Quality Standards for O(3) (0.08 ppm for 8 hr) indicate that above the present natural background levels, there is almost no safety margin for the effects of ambient O(3) on airway permeability. The assay of CC16 in the serum represents a new sensitive noninvasive test allowing the detection of early effects of ambient O(3) on the lung epithelial barrier.ImagesFigure 1Figure 2Figure 3

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Section: Discussionmentioning

confidence: 99%

Serum clara cell protein: a sensitive biomarker of increased lung epithelium permeability caused by ambient ozone.

Broeckaert

Arsalane²,

Hermans³

et al. 2000

Environ Health Perspect

108

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“…The mechanisms through which ozone affects permeability are not well understood. Despite the observation that increased airway permeability is associated with the transit of inflammatory cells, principally neutrophils, into the airway lumen (4-6), a causal role for these cells is brought into question by the demonstration that ozone-induced permeability is not affected by neutrophil depletion (7,8) and that increased permeability and cellular influx can exhibit temporal separation (9). Alternatively, ozone may affect barrier integrity through direct action on epithelial cells by causing oxidation of membrane lipids or other cellular components (10,11), leading, in some cases, to the release of mediators (12,13).…”

mentioning

confidence: 99%

Modulation of Bronchial Epithelial Cell Barrier Function by in vitro Ozone Exposure

Yu¹,

Takahashi²,

Croxton³

et al. 1994

Environmental Health Perspectives

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Alteration of alveolar macrophage chemotaxis, cell adhesion, and cell adhesion molecules following ozone exposure of rats

Bhalla¹

1996

J. Cell. Physiol.

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Ozone (O3) exposure of humans and animals induces an inflammatory response in the lung, which is associated with macrophage stimulation, release of chemotactic agents, and recruitment of polymorphonuclear leukocytes (PMNs). This study was designed to investigate the functional aspects of the macrophages that impact inflammatory processes in the lung. Macrophages recovered by bronchoalveolar lavage (BAL) from rats exposed to purified air or 0.8 ppm O3 were studied for their chemotactic activity, adhesive interactions with alveolar epithelial cells in culture, surface morphology, and surface expression of cell adhesion molecules. The macrophages isolated from O3-exposed rats exhibited a greater motility in response to a chemotactic stimulus than the macrophages isolated from rats exposed to purified air. The macrophages from O3-exposed animals also displayed greater adhesion when placed in culture with epithelial cells isolated from adult rat lung (ARL-14) than the macrophages from control rats. Both chemotactic motility and cell adhesion stimulated by O3 exposure were attenuated when the macrophages were incubated in the presence of monoclonal antibodies to leukocyte adhesion molecules, CD11b, or epithelial cell adhesion molecules, ICAM-1. Flow cytometry revealed a modest increase in the surface expression of CD11b but no change in ICAM-1 expression in macrophages from O3-exposed rats when compared to those from the air-exposed controls. The results demonstrate an alteration of macrophage functions following O3 exposure and suggest the dependence of these functions on the biologic characteristics, rather than the absolute expression, of the cell adhesion molecules.

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Time course of permeability changes and PMN flux in rat trachea following O3 exposure

Cited by 16 publications

References 18 publications

Serum clara cell protein: a sensitive biomarker of increased lung epithelium permeability caused by ambient ozone.

Serum clara cell protein: a sensitive biomarker of increased lung epithelium permeability caused by ambient ozone.

Modulation of Bronchial Epithelial Cell Barrier Function by in vitro Ozone Exposure

Alteration of alveolar macrophage chemotaxis, cell adhesion, and cell adhesion molecules following ozone exposure of rats

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