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Acute cigarette smoke exposure induces apoptosis of alveolar macrophages

K Aoshiba1, J Tamaoki, A Nagai

  • 1First Department of Medicine, Tokyo Women's Medical University, Shinjuku-ku, Tokyo 162-8666, Japan. kaoshiba@chi.twmu.ac.jp

American Journal of Physiology. Lung Cellular and Molecular Physiology
|November 13, 2001
PubMed

Insights

Cigarette smoke (CS) triggers apoptosis, or programmed cell death, in alveolar macrophages (AMs). Antioxidants can prevent this effect, suggesting a role for oxidative stress in CS-induced lung injury.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Toxicology

Background:

  • Alveolar macrophages (AMs) are crucial in lung health and disease.
  • Cigarette smoke (CS) is a major risk factor for pulmonary diseases.

Purpose of the Study:

  • To investigate if CS exposure induces apoptosis in AMs.
  • To elucidate the mechanisms underlying CS-induced AM apoptosis.

Main Methods:

  • In vitro studies using mouse, rat, and human AMs exposed to CS extracts.
  • In vivo rat model exposed to CS.
  • Apoptosis detection via microscopy and TUNEL assay.
  • Analysis of oxidative stress, mitochondrial function, and key proteins (Bax, p53, caspases).

Main Results:

  • Aqueous CS extracts induced apoptosis in all tested AMs, but the gas phase did not.
  • CS-induced apoptosis involved oxidative stress, Bax accumulation, and mitochondrial dysfunction, independent of p53, Fas, and caspase activation.
  • Antioxidants (glutathione, ascorbic acid, alpha-tocopherol) inhibited CS-induced apoptosis.
  • In vivo CS exposure resulted in approximately 3% AM apoptosis.

Conclusions:

  • Acute CS exposure induces AM apoptosis.
  • Oxidative stress and mitochondrial pathways are key mediators of CS-induced AM apoptosis.
  • Targeting oxidative stress may offer therapeutic potential for CS-related lung diseases.

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