Functional alterations of alveolar macrophages subjected to smoke exposure and antioxidant lazaroids

Shengjun Wang, Robert Clark Lantz, Mary W. Vermeulen, Guan Jie Chen, Veronica Breceda, Raymond F. Robledo, Allison M. Hays, Scott Young, Mark L. Witten

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Acute inhalation of diesel fuel-polycarbonate plastic (DFPP) smoke causes severe lung injury, leading to acute respiratory distress syndrome (ARDS) and death. It has been reported that the initiation of acute lung injury is associated with the activation of pulmonary alveolar macrophages (PAM). To further explore the pathogenesis, alveolar macrophages (AM) of New Zealand rabbits ventilated and exposed to a 60 tidal volume of DFPP smoke in vivo were recovered at I h post-smoke. Smoke exposure induced significant increases in both mRNA and protein levels for PAM tumor necrosis factor-α (TNF-α), when compared to smoke control. Smoke also induced a biphasic response (inhibited at 2 h, enhanced at 24 h after cell isolation) in the production of superoxide (O2-) by PAM. However, aerosolized lazaroid, U75412E (1.6 mg/kg body weight), significantly attenuated smoke-induced expression in AM TNF-α at the protein level but not at the mRNA level, and smoke-induced changes in AM production of O2-. This study suggests that highly expressing AM TNF-α following smoke may be a key contributor to the cascade that establishes an acute injury process and exacerbates oxidant- derived cell injury. Whereas, the lazaroid may ameliorate smoke-induced lung injury by attenuating AM TNF-α release, in addition to its primary antioxidative mechanism.

Original languageEnglish (US)
Pages (from-to)464-469
Number of pages6
JournalToxicology and Industrial Health
Volume15
Issue number5
StatePublished - Aug 1999

Fingerprint

Alveolar Macrophages
Smoke
Antioxidants
Tumor Necrosis Factor-alpha
Gasoline
Diesel fuels
Lung Injury
Messenger RNA
Cell Separation
Acute Lung Injury
Tidal Volume
Adult Respiratory Distress Syndrome
Wounds and Injuries
Oxidants
Superoxides
Inhalation
Proteins
Chemical activation
Body Weight
Rabbits

Keywords

  • Alveolar macrophages
  • Lazaroids
  • Lung injury
  • Smoke inhalation
  • Superoxide
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Wang, S., Lantz, R. C., Vermeulen, M. W., Chen, G. J., Breceda, V., Robledo, R. F., ... Witten, M. L. (1999). Functional alterations of alveolar macrophages subjected to smoke exposure and antioxidant lazaroids. Toxicology and Industrial Health, 15(5), 464-469.

Functional alterations of alveolar macrophages subjected to smoke exposure and antioxidant lazaroids. / Wang, Shengjun; Lantz, Robert Clark; Vermeulen, Mary W.; Chen, Guan Jie; Breceda, Veronica; Robledo, Raymond F.; Hays, Allison M.; Young, Scott; Witten, Mark L.

In: Toxicology and Industrial Health, Vol. 15, No. 5, 08.1999, p. 464-469.

Research output: Contribution to journalArticle

Wang, S, Lantz, RC, Vermeulen, MW, Chen, GJ, Breceda, V, Robledo, RF, Hays, AM, Young, S & Witten, ML 1999, 'Functional alterations of alveolar macrophages subjected to smoke exposure and antioxidant lazaroids', Toxicology and Industrial Health, vol. 15, no. 5, pp. 464-469.
Wang, Shengjun ; Lantz, Robert Clark ; Vermeulen, Mary W. ; Chen, Guan Jie ; Breceda, Veronica ; Robledo, Raymond F. ; Hays, Allison M. ; Young, Scott ; Witten, Mark L. / Functional alterations of alveolar macrophages subjected to smoke exposure and antioxidant lazaroids. In: Toxicology and Industrial Health. 1999 ; Vol. 15, No. 5. pp. 464-469.
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