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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1990-3-23
|
| pubmed:abstractText |
Infective mortality is common in children who have hepatic failure. We have demonstrated that experimental hepatic failure (EHF) profoundly suppresses T cell function in vivo. To determine the basis for immune suppression in EHF we postulated that this phenomenon is attributable to alterations in accessory macrophage (Ma) function, T cell subsets, interleukin-2 (IL-2) production, or serum inhibition. Wistar Furth rats (200 g) were randomized to EHF (n = 23), Sham (n = 23), and normal control (NC) (n = 23) groups. On day 21, splenocytes and sera were harvested and immune assays performed in vitro. Following are the results (mean +/- SEM; Student's t test). Serum bilirubin was elevated in EHF versus Sham and NC groups (P less than .01). EHF splenic macrophages suppressed PHA when added to microcultures at 10(5) concentration (-140 +/- 550 v 12,263 +/- 2,492 [Sham] and 21,413 +/- 1,702 [NC] P less than .01). This effect was not evident when macrophages were added back to microcultures at 10(3) and 10(4) concentrations, suggesting a dose-dependent inhibitory effect. T helper: suppressor ratios did not differ in EHF (1.3 +/- 0.2) compared with Sham (1.4 +/- 0.2) and NC groups (1.2 +/- 0.1). IL-2 production was similar in EHF, Sham, and NC animals (112,141 +/- 5,232 versus 106,691 +/- 1,419 and 120,759 +/- 3,249 counts per minute). T cell inhibitory activity was not demonstrable in EHF sera. These data show that splenic macrophages can inhibit T cell function in vitro. This phenomenon may be paramount in predisposing children with liver disease to infection.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
0022-3468
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
25
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
204-7
|
| pubmed:dateRevised |
2005-11-17
|
| pubmed:meshHeading |
pubmed-meshheading:2137536-Animals,
pubmed-meshheading:2137536-Cholestasis,
pubmed-meshheading:2137536-Female,
pubmed-meshheading:2137536-Interleukin-2,
pubmed-meshheading:2137536-Leukocyte Count,
pubmed-meshheading:2137536-Liver Diseases,
pubmed-meshheading:2137536-Lymphocyte Activation,
pubmed-meshheading:2137536-Macrophages,
pubmed-meshheading:2137536-Phytohemagglutinins,
pubmed-meshheading:2137536-Rats,
pubmed-meshheading:2137536-Rats, Inbred WF,
pubmed-meshheading:2137536-Spleen,
pubmed-meshheading:2137536-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:2137536-T-Lymphocytes, Regulatory
|
| pubmed:year |
1990
|
| pubmed:articleTitle |
A potential basis for suppressed inflammatory cell function in pediatric cholestatic hosts.
|
| pubmed:affiliation |
Department of Surgery, University of Texas Medical School, Houston 77030.
|
| pubmed:publicationType |
Journal Article
|