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PMID: 9358756 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Role of tumor necrosis factor-alpha in the spontaneous development of pulmonary fibrosis in viable motheaten mutant mice.

The American journal of pathology ·Vol. 151 ·No. 5 ·1997-11-00 ·Pages 1303-10

Thrall RS, Vogel SN, Evans R, Shultz LD

Abstract

The viable motheaten mutant mouse is severely immunodeficient and dies from a naturally occurring progressive pulmonary inflammation at approximately 10 weeks of age. The pulmonary disease is characterized by excessive macrophage accumulation in the lung and fibrosis. We correlated the development of lung injury in viable motheaten mice with tumor necrosis factor-alpha (TNF-alpha) levels in serum and lung. Significantly increased serum TNF-alpha levels were observed by enzyme-linked immunosorbent assay in viable motheaten mice at 4, 6, and 10 weeks of age as compared with normal control littermate mice. These ages correlated well with observed changes in lung wet weights, lung collagen content, and histological evidence of pulmonary inflammation and fibrosis. Qualitative assessment of lung tissue TNF-alpha levels was performed by immunohistochemical staining using immunoperoxidase techniques. These studies revealed increased levels of TNF-alpha in macrophage-like cells in viable motheaten mice from 5 to 10 weeks of age as compared with littermate control animals. Alveolar macrophages isolated from viable motheaten mice produced significantly greater amounts of TNF-alpha when stimulated with lipopolysaccharide compared with alveolar macrophages from control animals. In addition, administration of anti-TNF-alpha antibody to motheaten bone marrow recipient mice decreased the severity of acute lung injury. The results demonstrate a close correlation between the development of pulmonary injury and TNF-alpha levels in this model of spontaneously developing fibrotic lung disease.

MeSH Terms
Animals Bone Marrow Transplantation Cells, Cultured Chimera/drug effects Immune Tolerance/physiology Immunization, Passive Immunoenzyme Techniques Lung/metabolism,pathology Macrophages, Alveolar/metabolism Mice Mice, Inbred C57BL Mice, Mutant Strains/genetics Pulmonary Fibrosis/genetics,metabolism,pathology Tumor Necrosis Factor-alpha/immunology,metabolism,physiology
Chemicals
Tumor Necrosis Factor-alpha
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Thrall R S
Pulmonary Division, University of Connecticut Health Center, Farmington, USA.
Vogel S N
Evans R
Shultz L D
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Article Info
Journal
The American journal of pathology
Abbr.
Am J Pathol
ISSN
0002-9440
Published
1997-11-00
Pages
1303-10
Language
English
Region
United States
NLM ID
0370502
PMCID
PMC1858072
Subset
IM
Grants
NIAID NIH HHS · AI 18797 · United States
NCI NIH HHS · CA 20408 · United States
NHLBI NIH HHS · HL 39939 · United States
External Links
PubMed source PMC Full Text View journal details
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