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Lung

, Volume 176, Issue 5, pp 325–336 | Cite as

Cotton Smoke Inhalation Primes Alveolar Macrophages for Tumor Necrosis Factor-α Production and Suppresses Macrophage Antimicrobial Activities

  • A.  Bidani
  • C. Z.  Wang
  • T. A.  Heming

Abstract.

The present study determined the effects of cotton smoke inhalation on the functioning of alveolar macrophages (mφ). Smoke inhalation led to dose-dependent impairment of respiratory gas exchange by 48 h postexposure and pulmonary edema by 96 h. Maximal effects were observed in animals ventilated with 54 breaths of cotton smoke (3-min exposure, 18 breaths/min). Macrophages were obtained at 48 h postexposure by bronchoalveolar lavage of rabbits subjected to 54 breaths of smoke or room air (control). Phagocytosis of opsonized bacteria and adherence to solid substratum were reduced in smoke-exposed mφ. Smoke inhalation primed mφ for release of tumor necrosis factor-α (TNF-α) induced by lipopolysaccharide (LPS). Smoke-exposed mφ were also primed for TNF-α release induced by phorbol myristate acetate, which suggests that the priming event occurred downstream of protein kinase C activation in the signal transduction pathway. Further, smoke exposure attenuated the inhibitory effects of phosphodiesterase inhibitors on LPS-induced TNF-α release. Thus, the priming event may be mediated through cAMP and/or protein kinase A. The data indicate that cotton smoke inhalation suppresses the antimicrobial activities of alveolar mφ and can lead to excessive mφ production of TNF-α. These mφ effects would be expected to contribute to the pathophysiological abnormalities associated with smoke inhalation injury.

Key words: Tumor necrosis factor-α—Phagocytosis—Acute lung injury—Rabbit. 

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Copyright information

© Springer-Verlag New York Inc. 1998

Authors and Affiliations

  • A.  Bidani
    • 1
  • C. Z.  Wang
    • 1
  • T. A.  Heming
    • 1
  1. 1.Departments of Internal Medicine, and Physiology and Biophysics, University of Texas Medical Branch, Galveston, Texas 77555-0876, USAUS

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