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Tumor necrosis factor-alpha-induced lung injury and its modulation by synthetic polynucleotide: a physiologic-morphometric analysis.

Publication ,  Journal Article
Huang, YC; Fracica, PJ; Piantadosi, CA
Published in: Exp Lung Res
1994

PolyI:C, a potent interferon (IFN) inducer, protects the isolated perfused lung (IPL) against platelet-activating factor (PAF)-induced injury. Because the release of PAF is stimulated by tumor necrosis factor (TNF), this study was designed to measure the effects of polyI:C on TNF-induced lung inflammation and injury. TNF (2.5 micrograms/kg) was administered to rabbits intravenously as continuous infusion over 2 h. PolyI:C was given intraperitoneally 16 h before TNF infusion. The rabbits were then anesthetized and sacrificed, and the lungs were ventilated with 20% O2 + 5% CO2 and perfused with buffer for 60 min. Lung weight gain was recorded continuously. After perfusion, lungs were inflation fixed for light and electron microscopy with morphometric analysis. Four groups of rabbit lungs were studied: (1) control; (2) polyI:C; (3) TNF, and (4) polyI:C + TNF. Lungs in the TNF group showed increased weight gain (15.4 +/- 2.4 g/h vs. 7.1 +/- 0.5 g/h in controls, p = .02) and increased volume of inflammatory cells (261% of control). These were mostly mononuclear cells (96%), primarily located in the interstitial and alveolar compartments (80%). In the polyI:C + TNF group, the weight gain of the IPL tended to be smaller (8.3 +/- 1.8 g/h, p = .08). Total inflammatory cell volume in the IPL remained elevated (330% of control), but mononuclear cells accounted for only 60% of the cell population. Most of these cells were found in the intravascular compartment (65%) implicating mononuclear cells in the early pathogenesis of TNF-induced pulmonary capillary injury in rabbits. PolyI:C, which attenuates TNF-induced injury, also modulates effects of TNF on mononuclear cell and granulocyte infiltration in the lung.

Duke Scholars

Published In

Exp Lung Res

DOI

ISSN

0190-2148

Publication Date

1994

Volume

20

Issue

6

Start / End Page

539 / 558

Location

England

Related Subject Headings

  • Vascular Resistance
  • Tumor Necrosis Factor-alpha
  • Respiratory System
  • Recombinant Proteins
  • Rabbits
  • Pulmonary Edema
  • Pulmonary Circulation
  • Poly I-C
  • Peroxidase
  • Perfusion
 

Citation

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MLA
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Huang, Y. C., Fracica, P. J., & Piantadosi, C. A. (1994). Tumor necrosis factor-alpha-induced lung injury and its modulation by synthetic polynucleotide: a physiologic-morphometric analysis. Exp Lung Res, 20(6), 539–558. https://doi.org/10.3109/01902149409031736
Huang, Y. C., P. J. Fracica, and C. A. Piantadosi. “Tumor necrosis factor-alpha-induced lung injury and its modulation by synthetic polynucleotide: a physiologic-morphometric analysis.Exp Lung Res 20, no. 6 (1994): 539–58. https://doi.org/10.3109/01902149409031736.
Huang, Y. C., et al. “Tumor necrosis factor-alpha-induced lung injury and its modulation by synthetic polynucleotide: a physiologic-morphometric analysis.Exp Lung Res, vol. 20, no. 6, 1994, pp. 539–58. Pubmed, doi:10.3109/01902149409031736.
Journal cover image

Published In

Exp Lung Res

DOI

ISSN

0190-2148

Publication Date

1994

Volume

20

Issue

6

Start / End Page

539 / 558

Location

England

Related Subject Headings

  • Vascular Resistance
  • Tumor Necrosis Factor-alpha
  • Respiratory System
  • Recombinant Proteins
  • Rabbits
  • Pulmonary Edema
  • Pulmonary Circulation
  • Poly I-C
  • Peroxidase
  • Perfusion