Linked Life Data

11180269

Source:http://linkedlifedata.com/resource/pubmed/id/11180269

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-2-22
pubmed:abstractText
In recent immunological studies, it has been suggested that trichloroethylene (TCE) participates in the onset of pneumatosis cystoides intestinalis (PCI) through a certain mechanism; however, the mechanism by which it develops remains unknown. Based on findings that secondary PCI is often linked with autoimmune disease, the possibility that some genetic or immunological mechanisms are involved in the development of PCI has been proposed. Pneumatosis cystoides intestinalis is not a type of disease where a dose-response relationship with TCE exposure can be recognized and it is difficult to reproduce its physiopathology through TCE exposure in ordinary experimental animals. In the present study, immunological changes caused by TCE exposure were investigated by employing MRL-lpr/lpr mice that are genetically labile to autoimmune diseases. To observe changes in B cell functions, serum antibody titres were measured; and for the T cell function, T cell subsets were examined. The animals were exposed to TCE at dosages of 0, 500, 1000 and 2000 ppm through inhalation 4 h a day, 6 days a week, for 8 weeks. It was found that only IgG production capacity was suppressed and there were no changes in T cell subsets with TCE concentrations up to 1000 ppm. At a concentration of 2000 ppm, changes were noted in both T and B cell functions. Typical organs that are responsible for immunological functions were examined for their morphological changes under a light microscope: the spleen and liver exhibited dose-response changes at a concentration of 500 ppm or greater. The development of immunoblastoid cells at a concentration of 1000 ppm indicated a possibility that a change has occurred in the immunological system. These findings show that exposure to TCE at high concentrations affects the immune system, but the study failed to induce PCI in the experimental animals. Further studies on TCE exposure at lower concentrations for longer periods are needed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0260-437X
pubmed:author
pubmed:copyrightInfo
Copyright 2000 John Wiley & Sons, Ltd.
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
471-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Immunotoxicity of trichloroethylene: a study with MRL-lpr/lpr mice.
pubmed:affiliation
Department of Environmental Health, Medical University of Yamanashi, Shimokato 1110, Tamaho, Yamanashi 409-3898, Japan. tkaneko@res.yamanashi-med.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't