Sensitization of rat alveolar macrophages to enhanced TNF-α release by in vivo treatment with dexamethasone
Treatment of rats with dexamethasone rapidly induced a marked weight loss which occurred within 3 days and persisted for several weeks. The cachectic state was paralleled by increased serum levels of triglycerides, albumin, and protein and a strong reduction of blood mononuclear leukocytes. In lung...
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| Veröffentlicht in: | Cellular immunology 1992-10, Vol.144 (2), p.249-257 |
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| container_title | Cellular immunology |
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| creator | Renz, H. Henke, A. Hofmann, P. Wolff, L.J. Schmidt, A. Rüschoff, J. Gemsa, D. |
| description | Treatment of rats with dexamethasone rapidly induced a marked weight loss which occurred within 3 days and persisted for several weeks. The cachectic state was paralleled by increased serum levels of triglycerides, albumin, and protein and a strong reduction of blood mononuclear leukocytes. In lung sections, an increased number of mononuclear giant cells was found but no bacteria, fungi, or
Pneumocystis carinii organisms. Quite strikingly, alveolar macrophages from dexamethasone-treated rats, but not from control animals, were highly sensitive to LPS and released large amounts of TNF-α
ex vivo. Also under
in vivo conditions, high TNF-α serum concentrations were found in dexamethasone-treated but not control rats when examined
1
1
2
hr after an intravenous LPS injection. These data, suggest that the glucocorticoid-induced cachexia of rats may be linked, at least in part, to readily inducible TNF-α release from primed macrophages. |
| doi_str_mv | 10.1016/0008-8749(92)90242-H |
| format | Article |
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Pneumocystis carinii organisms. Quite strikingly, alveolar macrophages from dexamethasone-treated rats, but not from control animals, were highly sensitive to LPS and released large amounts of TNF-α
ex vivo. Also under
in vivo conditions, high TNF-α serum concentrations were found in dexamethasone-treated but not control rats when examined
1
1
2
hr after an intravenous LPS injection. These data, suggest that the glucocorticoid-induced cachexia of rats may be linked, at least in part, to readily inducible TNF-α release from primed macrophages.</description><identifier>ISSN: 0008-8749</identifier><identifier>EISSN: 1090-2163</identifier><identifier>DOI: 10.1016/0008-8749(92)90242-H</identifier><identifier>PMID: 1394443</identifier><identifier>CODEN: CLIMB8</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Dexamethasone - pharmacology ; Dinoprostone - biosynthesis ; Female ; Immunomodulators ; Lipopolysaccharides ; Macrophages, Alveolar - drug effects ; Macrophages, Alveolar - metabolism ; Medical sciences ; Pharmacology. Drug treatments ; Rats ; Rats, Inbred Lew ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Tumor Necrosis Factor-alpha - physiology ; Weight Loss - drug effects</subject><ispartof>Cellular immunology, 1992-10, Vol.144 (2), p.249-257</ispartof><rights>1992</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c332t-c9db8e5f4a3f2b09c1632781a8c6db834bbb05b8f4872478f480641945e528423</citedby><cites>FETCH-LOGICAL-c332t-c9db8e5f4a3f2b09c1632781a8c6db834bbb05b8f4872478f480641945e528423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0008-8749(92)90242-H$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4444600$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1394443$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Renz, H.</creatorcontrib><creatorcontrib>Henke, A.</creatorcontrib><creatorcontrib>Hofmann, P.</creatorcontrib><creatorcontrib>Wolff, L.J.</creatorcontrib><creatorcontrib>Schmidt, A.</creatorcontrib><creatorcontrib>Rüschoff, J.</creatorcontrib><creatorcontrib>Gemsa, D.</creatorcontrib><title>Sensitization of rat alveolar macrophages to enhanced TNF-α release by in vivo treatment with dexamethasone</title><title>Cellular immunology</title><addtitle>Cell Immunol</addtitle><description>Treatment of rats with dexamethasone rapidly induced a marked weight loss which occurred within 3 days and persisted for several weeks. The cachectic state was paralleled by increased serum levels of triglycerides, albumin, and protein and a strong reduction of blood mononuclear leukocytes. In lung sections, an increased number of mononuclear giant cells was found but no bacteria, fungi, or
Pneumocystis carinii organisms. Quite strikingly, alveolar macrophages from dexamethasone-treated rats, but not from control animals, were highly sensitive to LPS and released large amounts of TNF-α
ex vivo. Also under
in vivo conditions, high TNF-α serum concentrations were found in dexamethasone-treated but not control rats when examined
1
1
2
hr after an intravenous LPS injection. These data, suggest that the glucocorticoid-induced cachexia of rats may be linked, at least in part, to readily inducible TNF-α release from primed macrophages.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Dexamethasone - pharmacology</subject><subject>Dinoprostone - biosynthesis</subject><subject>Female</subject><subject>Immunomodulators</subject><subject>Lipopolysaccharides</subject><subject>Macrophages, Alveolar - drug effects</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><subject>Weight Loss - drug effects</subject><issn>0008-8749</issn><issn>1090-2163</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQhy0EKkvhDUDyASE4BMZ_ktgXJFTRLlIFB8rZcpwJa5TEi-1daN-KF-GZcLqrcoPTHH7fjGa-IeQpg9cMWPMGAFSlWqlfav5KA5e8Wt8jKwYaKs4acZ-s7pCH5FFK3wAYkxpOyAkTWkopVmT8jHPy2d_Y7MNMw0CjzdSOewyjjXSyLobtxn7FRHOgOG_s7LCnVx_Pq9-_aMQRbULaXVM_073fB5oj2jzhnOkPnze0x592wryxKcz4mDwY7JjwybGeki_n76_O1tXlp4sPZ-8uKycEz5XTfaewHqQVA-9Au3IMbxWzyjUlEbLrOqg7NUjVctkuFRrJtKyx5kpycUpeHOZuY_i-w5TN5JPDcbQzhl0yreDANMB_QdZIVTesLaA8gEVHShEHs41-svHaMDDLN8yi2iyqjebm9htmXdqeHefvugn7v00H_SV_fsxtcnYcYrHr0x1WGNncrvn2gGGRtvcYTXIel0f4iC6bPvh_7_EHTkCmpg</recordid><startdate>19921015</startdate><enddate>19921015</enddate><creator>Renz, H.</creator><creator>Henke, A.</creator><creator>Hofmann, P.</creator><creator>Wolff, L.J.</creator><creator>Schmidt, A.</creator><creator>Rüschoff, J.</creator><creator>Gemsa, D.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19921015</creationdate><title>Sensitization of rat alveolar macrophages to enhanced TNF-α release by in vivo treatment with dexamethasone</title><author>Renz, H. ; Henke, A. ; Hofmann, P. ; Wolff, L.J. ; Schmidt, A. ; Rüschoff, J. ; Gemsa, D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c332t-c9db8e5f4a3f2b09c1632781a8c6db834bbb05b8f4872478f480641945e528423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Dexamethasone - pharmacology</topic><topic>Dinoprostone - biosynthesis</topic><topic>Female</topic><topic>Immunomodulators</topic><topic>Lipopolysaccharides</topic><topic>Macrophages, Alveolar - drug effects</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Medical sciences</topic><topic>Pharmacology. 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The cachectic state was paralleled by increased serum levels of triglycerides, albumin, and protein and a strong reduction of blood mononuclear leukocytes. In lung sections, an increased number of mononuclear giant cells was found but no bacteria, fungi, or
Pneumocystis carinii organisms. Quite strikingly, alveolar macrophages from dexamethasone-treated rats, but not from control animals, were highly sensitive to LPS and released large amounts of TNF-α
ex vivo. Also under
in vivo conditions, high TNF-α serum concentrations were found in dexamethasone-treated but not control rats when examined
1
1
2
hr after an intravenous LPS injection. These data, suggest that the glucocorticoid-induced cachexia of rats may be linked, at least in part, to readily inducible TNF-α release from primed macrophages.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>1394443</pmid><doi>10.1016/0008-8749(92)90242-H</doi><tpages>9</tpages></addata></record> |
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| ispartof | Cellular immunology, 1992-10, Vol.144 (2), p.249-257 |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Animals Biological and medical sciences Dexamethasone - pharmacology Dinoprostone - biosynthesis Female Immunomodulators Lipopolysaccharides Macrophages, Alveolar - drug effects Macrophages, Alveolar - metabolism Medical sciences Pharmacology. Drug treatments Rats Rats, Inbred Lew Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Tumor Necrosis Factor-alpha - physiology Weight Loss - drug effects |
| title | Sensitization of rat alveolar macrophages to enhanced TNF-α release by in vivo treatment with dexamethasone |
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