Increased tumor necrosis factor-alpha (TNF-alpha) gene expression in parainfluenza type 1 (Sendai) virus-induced bronchiolar fibrosis.
Identifieur interne : 001190 ( Main/Exploration ); précédent : 001189; suivant : 001191Increased 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.
Url:
PubMed: 9466578
PubMed Central: 1857970
Affiliations:
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Le document en format XML
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W." last="Uhl">E. W. Uhl</name></author><author><name sortKey="Moldawer, L L" sort="Moldawer, L L" uniqKey="Moldawer L" first="L. L." last="Moldawer">L. L. Moldawer</name></author><author><name sortKey="Busse, W W" sort="Busse, W W" uniqKey="Busse W" first="W. W." last="Busse">W. W. Busse</name></author><author><name sortKey="Jack, T J" sort="Jack, T J" uniqKey="Jack T" first="T. J." last="Jack">T. J. Jack</name></author><author><name sortKey="Castleman, W L" sort="Castleman, W L" uniqKey="Castleman W" first="W. L." last="Castleman">W. L. Castleman</name></author></analytic><series><title level="j">The American Journal of Pathology</title><idno type="ISSN">0002-9440</idno><idno type="eISSN">1525-2191</idno><imprint><date when="1998">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><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></div></front></TEI><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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