Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:3337461rdf:typepubmed:Citationlld:pubmed
pubmed-article:3337461lifeskim:mentionsumls-concept:C0273115lld:lifeskim
pubmed-article:3337461lifeskim:mentionsumls-concept:C0205470lld:lifeskim
pubmed-article:3337461lifeskim:mentionsumls-concept:C0077151lld:lifeskim
pubmed-article:3337461lifeskim:mentionsumls-concept:C2587213lld:lifeskim
pubmed-article:3337461lifeskim:mentionsumls-concept:C0205263lld:lifeskim
pubmed-article:3337461lifeskim:mentionsumls-concept:C0332120lld:lifeskim
pubmed-article:3337461pubmed:issue1lld:pubmed
pubmed-article:3337461pubmed:dateCreated1988-2-10lld:pubmed
pubmed-article:3337461pubmed:abstractTextTrimellitic anhydride (TMA) is a chemical intermediate that has been shown to cause immunologically mediated respiratory syndromes in humans. We developed a rat model in which lung lesions accompanied by TMA-specific antibody resembled effects seen in humans. Two sets of experiments were undertaken to determine if TMA lung injury was primarily controlled by the immune system. Experiment 1: Rats were exposed to 95 micrograms/m3 of TMA 6 h/day, 5 days/wk for 2 wk during which time they received daily injections of either the immunosuppressant cyclophosphamide or saline. The TMA-exposed/saline control rats exhibited the usual TMA-induced lung lesions accompanied by TMA-specific antibody. However, the TMA-exposed/cyclophosphamide rats showed no lesions and no antibody. The spleen cells from all rats were subjected to lymphocyte blastogenesis assays using T- and B-cell mitogens. Results confirmed that cyclophosphamide-treated rats showed very little if any blastogenic response, whereas saline-treated rats gave the normal immune response. Thus, cyclophosphamide eliminated T- and B-cell function, which in turn prevented the occurrence of TMA lesions. Experiment 2: An initial passive transfer experiment showed that serum from TMA-sensitized rats could be adoptively transferred into naive recipient rats, which when given a single TMA inhalation challenge exhibited TMA-induced lesions. Similar attempts to transfer spleen cells or spleen cells plus serum did not predispose recipients for lesions. A second modified passive transfer of sensitized serum using a larger number of recipient rats, followed by a TMA challenge, resulted in lesions in 14 of the 16 rats.(ABSTRACT TRUNCATED AT 250 WORDS)lld:pubmed
pubmed-article:3337461pubmed:languageenglld:pubmed
pubmed-article:3337461pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:3337461pubmed:citationSubsetAIMlld:pubmed
pubmed-article:3337461pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:3337461pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:3337461pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:3337461pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:3337461pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:3337461pubmed:statusMEDLINElld:pubmed
pubmed-article:3337461pubmed:monthJanlld:pubmed
pubmed-article:3337461pubmed:issn0003-0805lld:pubmed
pubmed-article:3337461pubmed:authorpubmed-author:ZeissC RCRlld:pubmed
pubmed-article:3337461pubmed:authorpubmed-author:HatoumN SNSlld:pubmed
pubmed-article:3337461pubmed:authorpubmed-author:GarvinP JPJlld:pubmed
pubmed-article:3337461pubmed:authorpubmed-author:RatajczakH...lld:pubmed
pubmed-article:3337461pubmed:authorpubmed-author:LeachC LCLlld:pubmed
pubmed-article:3337461pubmed:issnTypePrintlld:pubmed
pubmed-article:3337461pubmed:volume137lld:pubmed
pubmed-article:3337461pubmed:ownerNLMlld:pubmed
pubmed-article:3337461pubmed:authorsCompleteYlld:pubmed
pubmed-article:3337461pubmed:pagination186-90lld:pubmed
pubmed-article:3337461pubmed:dateRevised2003-11-14lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:meshHeadingpubmed-meshheading:3337461-...lld:pubmed
pubmed-article:3337461pubmed:year1988lld:pubmed
pubmed-article:3337461pubmed:articleTitleEvidence of immunologic control of lung injury induced by trimellitic anhydride.lld:pubmed
pubmed-article:3337461pubmed:affiliationIIT Research Institute, Veterans Administration Lakeside Medical Center, Chicago, IL 60616.lld:pubmed
pubmed-article:3337461pubmed:publicationTypeJournal Articlelld:pubmed