Ozone-Induced Modulation of Cell-Mediated Immune Responses in the Lungs

Cohen, Mitchell D.; Sisco, Maureen; Li, Yun; Zelikoff, Judith T.; Schlesinger, Richard B.

doi:10.1006/taap.2000.9106

Cited by 35 publications

(22 citation statements)

References 52 publications

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“…For the 1-wk exposures followed by instillation of 4 × 10 6 or 8 × 10 6 Listeria, bacterial burdens tended to be greater in lungs of rats exposed to O 3 compared to those of air controls. When the high Listeria dose was used, O 3 -exposed rats showed continual increases in burdens, rather than displaying a "peak-andresolve" pattern (wherein burdens reach a plateau at 3 days postinfection and then begin to decline) that we have observed repeatedly in other studies (i.e., Cohen et al, 2001) that examined the Listeria infection process in the lungs of control rats. At the lower infection dose, only 0.3 ppm O 3 -exposed rats displayed a similar pattern of increasing listeric burden; 0.1 ppmexposed rats began to display a more normal clearance pattern, though burdens were still greater than those in control rats.…”

Section: Effects Of Ozone On Lung Immune Cells 605mentioning

confidence: 60%

“…Rats in the 3-wk exposures received only the lower dose of bacteria. At 48 and 96 h postinfection, rat cohorts were sacrificed by phenobarbital overdose (120 mg/kg, ip) and the lungs were processed for determination of Listeria (Cohen et al, 2001). Clearance was calculated as change in burden as a function of time postinfection.…”

Section: Bacterial Clearancementioning

confidence: 99%

“…Exposure at levels normally encountered in outdoor air results in various functional alterations in the respiratory tract (U.S. EPA, 1996). However, effects of O 3 on relatively specific aspects of pulmonary or systemic immune systems have been examined only to a limited extent (e.g., see Cohen et al, 2001). The available data do suggest that T-lymphocyte (cell-mediated) immunity (CMI) in host defense against infectious agents is more susceptible to O 3 than B-lymphocyte (i.e., humoral) immunity (Ryan, 2000).…”

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confidence: 97%

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Effects of Inhaled Ozone on Pulmonary Immune Cells Critical to Antibacterial Responses in Situ

Cohen

Sisco

Baker

et al. 2002

Inhalation Toxicology

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The goal of this study was to examine effects from repeated exposure to ozone (O 3 ) on immune cells involved in cell-mediated antibacterial responses in the lungs. Rats exposed to 0.1 or 0.3 ppm O 3 for 4 h/ day, 5 days/ wk, for 1 or 3 wk were analyzed for the ability to clear an intrapulmonary challenge with Listeria monocytogenes or had their lungs processed to obtain pulmonary alveolar macrophages (PAM) and lung-associated lymphocytes for analyses of select cell functions and surface marker expression. The results indicate that repeated inhalation exposure to O 3 affected local cell-mediated immunity ( CMI) responses as evidenced by effects on clearance of Listeria. However, this modulation was not consistently dependent on exposure concentration or duration. Short-term repeat exposures had more effect on host resistance than did the more prolonged regimen, with rats exposed to 0.1 ppm O 3 most adversely impacted. Clearance patterns suggest modifications in innate resistance following 1 wk of exposure to 0.1 ppm O 3 , but no similar effect following a 3-wk regimen. Exposure to 0.3 ppm O 3 appeared to affect both innate and acquired resistance after a 1-wk regimen, but mainly the former after an additional 2 wk of exposure. We conclude that these two mechanisms of resistance are differentially affected by O 3 and that distinct time-and O 3 concentration-dependent adaptation phenomena evolve for each; that is, in situ adaptation to higher levels of O 3 may occur more readily with acquired than with innate/ PAM-dependent resistance. A similar pattern of inconsistent effect on PAM and lung-associated lymphocytes was also evident. For example, while 3-wk exposures had a greater effect on PAM reactive oxygen intermediate ROI production, evidence 599

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Section: Effects Of Ozone On Lung Immune Cells 605mentioning

confidence: 60%

Section: Bacterial Clearancementioning

confidence: 99%

mentioning

confidence: 97%

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Effects of Inhaled Ozone on Pulmonary Immune Cells Critical to Antibacterial Responses in Situ

Cohen

Sisco

Baker

et al. 2002

Inhalation Toxicology

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“…In humans with asthma, IL-1b is present in lavage, epithelial cells, and alveolar macrophages (28)(29)(30)(31). Ozone interacts with airway epithelium and alveolar macrophages to produce inflammation via increasing inflammatory cytokines, including IL-1b (29,(32)(33)(34)(35). The role of IL-1b in ozone-induced airway hyperreactivity has been suggested, since an IL-1 receptor antagonist, anakinra, prevents airway hyperreactivity and inflammation in ozoneexposed mice (36,37).…”

mentioning

confidence: 99%

IL-1 Receptors Mediate Persistent, but Not Acute, Airway Hyperreactivity to Ozone in Guinea Pigs

Verhein¹,

Jacoby

Fryer

2008

Am J Respir Cell Mol Biol

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Ozone exposure in the lab and environment causes airway hyperreactivity lasting at least 3 days in humans and animals. In guinea pigs 1 day after ozone exposure, airway hyperreactivity is mediated by eosinophils that block neuronal M 2 muscarinic receptor function, thus increasing acetylcholine release from airway parasympathetic nerves. However, mechanisms of ozone-induced airway hyperreactivity change over time, so that depleting eosinophils 3 days after ozone makes airway hyperreactivity worse rather than better. Ozone exposure increases IL-1b in bone marrow, which may contribute to acute and chronic airway hyperreactivity. To test whether IL-1b mediates ozone-induced airway hyperreactivity 1 and 3 days after ozone exposure, guinea pigs were pretreated with an IL-1 receptor antagonist (anakinra, 30 mg/kg, intraperitoneally) 30 minutes before exposure to filtered air or to ozone (2 ppm, 4 h). One or three days after exposure, airway reactivity was measured in anesthetized guinea pigs. The IL-1 receptor antagonist prevented ozoneinduced airway hyperreactivity 3 days, but not 1 day, after ozone exposure. Ozone-induced airway hyperreactivity was vagally mediated, since bronchoconstriction induced by intravenous acetylcholine was not changed by ozone. The IL-1 receptor antagonist selectively prevented ozone-induced reduction of eosinophils around nerves and prevented ozone-induced deposition of extracellular eosinophil major basic protein in airways. These data demonstrate that IL-1 mediates ozone-induced airway hyperreactivity at 3 days, but not 1 day, after ozone exposure. Furthermore, preventing hyperreactivity was accompanied by decreased eosinophil major basic protein deposition within the lung, suggesting that IL-1 affects eosinophil activation 3 days after ozone exposure.

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“…O 3 exposure reduces phagocytic ability of AM. Introduction of infectious agents such as S. zoopidemicus, L. monocytogenes and S. aureus in mouse models following acute O 3 exposure (0.1-0.8 ppm) results in decreased bacterial killing and increased morbidity and mortality due to infection (Cohen et al, 2001;Gilmour and Selgrade, 1993;Van Loveren et al, 1988). AM from humans exposed to 0.08 ppm O 3 for 6.6 h while exercising showed a decrease in phagocytic activity of 25% relative to control, while mice exposed to 0.8 ppm for 3 h showed a 42% decrease in phagocytosis (Selgrade et al, 1995).…”

Section: Lung Host Defensementioning

confidence: 98%

Volatile Organic Compounds from Pesticide Application and Contribution to Tropospheric Ozone

Marty

Spurlock

Barry

2010

Hayes' Handbook of Pesticide Toxicology

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Ozone-Induced Modulation of Cell-Mediated Immune Responses in the Lungs

Cited by 35 publications

References 52 publications

Effects of Inhaled Ozone on Pulmonary Immune Cells Critical to Antibacterial Responses in Situ

Effects of Inhaled Ozone on Pulmonary Immune Cells Critical to Antibacterial Responses in Situ

IL-1 Receptors Mediate Persistent, but Not Acute, Airway Hyperreactivity to Ozone in Guinea Pigs

Volatile Organic Compounds from Pesticide Application and Contribution to Tropospheric Ozone

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