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Tumor necrosis factor-alpha inhibits expression of pulmonary surfactant protein

J R Wispé1, J C Clark, B B Warner

  • 1University of Cincinnati, Department of Pediatrics, Ohio 45267-0541.

The Journal of Clinical Investigation
|December 1, 1990
PubMed

Insights

Tumor necrosis factor-alpha (TNF-alpha) inhibits pulmonary surfactant protein A (SP-A) and SP-B expression in lung cancer cells. This cytokine significantly reduces SP-A mRNA levels in a dose- and time-dependent manner.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Immunology

Background:

  • Pulmonary surfactant proteins (SP-A and SP-B) are crucial for lung function.
  • Tumor necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine implicated in various diseases.

Purpose of the Study:

  • To investigate the effect of TNF-alpha on the expression of SP-A and SP-B in human pulmonary adenocarcinoma cell lines.
  • To elucidate the molecular mechanisms underlying TNF-alpha's influence on surfactant protein synthesis.

Main Methods:

  • Exposure of pulmonary adenocarcinoma cell lines (H441-4) to varying concentrations and durations of TNF-alpha.
  • Quantification of SP-A and SP-B mRNA and protein levels using molecular biology techniques.
  • Assessment of cell viability and beta-actin mRNA to control for non-specific effects.

Main Results:

  • TNF-alpha significantly decreased SP-A content and mRNA levels in a dose- and time-dependent manner, reducing SP-A to <10% of control within 48 hours.
  • SP-A mRNA levels decreased within 12 hours, with near-complete loss after 24 hours, indicating pretranslational inhibition.
  • TNF-alpha also decreased SP-B mRNA levels but increased manganese superoxide dismutase (Mn-SOD) mRNA, while not affecting cell viability or growth.

Conclusions:

  • TNF-alpha exerts a marked pretranslational inhibitory effect on the expression of pulmonary surfactant proteins SP-A and SP-B in lung adenocarcinoma cells.
  • These findings suggest that macrophage-derived cytokines like TNF-alpha may play a role in regulating surfactant protein expression in the lung.

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