Increased tumor necrosis factor-alpha (TNF-alpha) gene expression in parainfluenza type 1 (Sendai) virus-induced bronchiolar fibrosis.
Identifieur interne : 000733 ( Pmc/Checkpoint ); précédent : 000732; suivant : 000734Increased tumor necrosis factor-alpha (TNF-alpha) gene expression in parainfluenza type 1 (Sendai) virus-induced bronchiolar fibrosis.
Auteurs : E. W. Uhl ; L. L. Moldawer ; W. W. Busse ; T. J. Jack ; W. L. CastlemanSource :
- The American Journal of Pathology [ 0002-9440 ] ; 1998.
Abstract
Increased airway resistance and airway hyperresponsiveness induced in rats by infection with parainfluenza type I (Sendai) virus is associated with bronchiolar fibrosis. To determine whether increased tumor necrosis factor (TNF)-alpha gene expression is an important regulatory event in virus-induced bronchiolar fibrosis, pulmonary TNF-alpha mRNA and protein expression was assessed in rat strains that are susceptible (Brown Norway; BN) and resistant (Fischer 344; F344) to virus-induced bronchiolar fibrosis. Virus-inoculated BN rats had increased TNF-alpha pulmonary mRNA levels (P < 0.05) and increased numbers of bronchiolar macrophages and fibroblasts expressing TNF-alpha protein compared with virus-inoculated F344 rats (P < 0.05). Virus inoculation also induced elevated TNF-alpha mRNA and protein levels (P < 0.05) in cultured rat alveolar macrophages (NR8383 cells). A 55-kd soluble TNF receptor-immunoglobulin G fusion protein (sTNFR-IgG) was used to inhibit TNF-alpha bioactivity in virus-inoculated BN rats. Treated rats had fewer proliferating bronchiolar fibroblasts, as detected by bromodeoxyuridine incorporation, compared with virus-inoculated control rats (P < 0.05). There was also increased mortality in p55sTNFR-IgG-treated virus-inoculated rats associated with increased viral replication and decreased numbers of macrophages and lymphocytes in bronchoalveolar lavage fluid (P < 0.05). The results of this study indicate that 1) Sendai virus can directly up-regulate TNF-alpha mRNA and protein expression in macrophages, 2) TNF-alpha is an important mediator of virus-induced bronchiolar fibrosis, and 3) TNF-alpha has a critical role in the termination of Sendai viral replication in the lung.
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PubMed: 9466578
PubMed Central: 1857970
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Pathol</journal-id><journal-title>The American Journal of Pathology</journal-title><issn pub-type="ppub">0002-9440</issn><issn pub-type="epub">1525-2191</issn></journal-meta><article-meta><article-id pub-id-type="pmid">9466578</article-id><article-id pub-id-type="pmc">1857970</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Increased tumor necrosis factor-alpha (TNF-alpha) gene expression in parainfluenza type 1 (Sendai) virus-induced bronchiolar fibrosis.</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Uhl</surname><given-names>E. W.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Moldawer</surname><given-names>L. L.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Busse</surname><given-names>W. W.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Jack</surname><given-names>T. J.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Castleman</surname><given-names>W. L.</given-names></name></contrib></contrib-group><aff>Department of Pathobiology, University of Florida, Gainesville 32610-0145, USA.</aff><pub-date pub-type="ppub"><month>2</month><year>1998</year></pub-date><volume>152</volume><issue>2</issue><fpage>513</fpage><lpage>522</lpage><abstract><p>Increased airway resistance and airway hyperresponsiveness induced in rats by infection with parainfluenza type I (Sendai) virus is associated with bronchiolar fibrosis. To determine whether increased tumor necrosis factor (TNF)-alpha gene expression is an important regulatory event in virus-induced bronchiolar fibrosis, pulmonary TNF-alpha mRNA and protein expression was assessed in rat strains that are susceptible (Brown Norway; BN) and resistant (Fischer 344; F344) to virus-induced bronchiolar fibrosis. Virus-inoculated BN rats had increased TNF-alpha pulmonary mRNA levels (P < 0.05) and increased numbers of bronchiolar macrophages and fibroblasts expressing TNF-alpha protein compared with virus-inoculated F344 rats (P < 0.05). Virus inoculation also induced elevated TNF-alpha mRNA and protein levels (P < 0.05) in cultured rat alveolar macrophages (NR8383 cells). A 55-kd soluble TNF receptor-immunoglobulin G fusion protein (sTNFR-IgG) was used to inhibit TNF-alpha bioactivity in virus-inoculated BN rats. Treated rats had fewer proliferating bronchiolar fibroblasts, as detected by bromodeoxyuridine incorporation, compared with virus-inoculated control rats (P < 0.05). There was also increased mortality in p55sTNFR-IgG-treated virus-inoculated rats associated with increased viral replication and decreased numbers of macrophages and lymphocytes in bronchoalveolar lavage fluid (P < 0.05). The results of this study indicate that 1) Sendai virus can directly up-regulate TNF-alpha mRNA and protein expression in macrophages, 2) TNF-alpha is an important mediator of virus-induced bronchiolar fibrosis, and 3) TNF-alpha has a critical role in the termination of Sendai viral replication in the lung.</p><sec sec-type="scanned-figures"><title>Images</title><fig id="F1"><label>Figure 2</label><graphic xlink:href="amjpathol00014-0190-a" xlink:role="517"></graphic></fig></sec></abstract></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Busse, W W" sort="Busse, W W" uniqKey="Busse W" first="W. W." last="Busse">W. W. Busse</name><name sortKey="Castleman, W L" sort="Castleman, W L" uniqKey="Castleman W" first="W. L." last="Castleman">W. L. Castleman</name><name sortKey="Jack, T J" sort="Jack, T J" uniqKey="Jack T" first="T. J." last="Jack">T. J. Jack</name><name sortKey="Moldawer, L L" sort="Moldawer, L L" uniqKey="Moldawer L" first="L. L." last="Moldawer">L. L. Moldawer</name><name sortKey="Uhl, E W" sort="Uhl, E W" uniqKey="Uhl E" first="E. W." last="Uhl">E. W. Uhl</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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