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Ozone-induced decrease of mouse tracheal potential is not secondary to cellular inflammation

M Takahashi1, S R Kleeberger, T L Croxton

  • 1Department of Environmental Health Sciences, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.

Toxicology and Applied Pharmacology
|March 1, 1995
PubMed
Summary
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Acute ozone exposure decreases tracheal electrical potential difference (PD) in mice. Inflammation is not required for this O3-induced PD response, suggesting other mechanisms are involved.

Area of Science:

  • Environmental Toxicology
  • Respiratory Physiology
  • Immunology

Background:

  • Acute exposure to ozone (O3), a major air pollutant, significantly impacts respiratory function.
  • Ozone inhalation is known to cause airway inflammation and alter tracheal electrical potential difference (PD).
  • The precise role of inflammatory cells in mediating O3-induced electrophysiological changes in the trachea remains unclear.

Purpose of the Study:

  • To investigate the role of inflammation in the O3-induced decrease in tracheal electrical potential difference (PD) in C57BL/6J (B6) mice.
  • To determine if inhibiting inflammatory responses affects the electrophysiological consequences of acute ozone exposure.

Main Methods:

  • Mice were pretreated with indomethacin, colchicine, or cyclophosphamide to modulate inflammatory responses.

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  • Mice were exposed to 2 ppm O3 or air for 3 hours, followed by recovery periods of 0-12 hours.
  • Tracheal PD was measured, and bronchoalveolar lavage (BAL) was performed to assess total cells, polymorphonuclear leukocytes (PMNs), and protein levels.

    • Main Results:

    • Ozone exposure decreased tracheal PD and increased BAL total cells, PMNs, and protein, with maximal effects observed 6-9 hours post-exposure.
    • Indomethacin pretreatment prevented the O3-induced decrease in PD but did not affect BAL inflammatory cell counts or protein.
    • Colchicine and cyclophosphamide, which inhibit PMN function and reduce inflammation, did not alter the O3-induced PD response.

    Conclusions:

    • The O3-induced decrease in tracheal PD is not dependent on cellular inflammation, particularly PMN infiltration.
    • The sensitivity of the PD response to indomethacin suggests a potential role for cyclooxygenase products in mediating this effect.
    • These findings indicate that non-inflammatory mechanisms are primarily responsible for the acute electrophysiological alterations in the trachea following ozone exposure.