Linked Life Data

11691656

Source:http://linkedlifedata.com/resource/pubmed/id/11691656

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-11-5
pubmed:abstractText
It is increasingly apparent that there is a bidirectional interaction between the maternal immune system and the reproductive system during pregnancy. Pregnancy is associated with a suppression of maternal specific immune responses, which process underlies the protection of fetal tissues expressing paternally inherited alloantigens. However, recent evidence indicates that the suppression of specific, lymphocyte-mediated immune responses during pregnancy is accompanied by activation of the non-specific arm of the maternal immune response. In the present study, we have investigated the effect of pregnancy on the non-specific immune response induced by bacterial lipopolysaccharide (LPS, endotoxin) in mice. Pregnancy enhanced the LPS-induced production of proinflammatory cytokines, including tumor necrosis factor-alpha, interleukin (IL)-6, and interferon-gamma. On the other hand, LPS-induced levels of the anti-inflammatory cytokine IL-10 were suppressed in pregnant mice. These alterations in cytokine production correlated with an increased susceptibility for endotoxemic mortality in the pregnant mice. Although adrenergic receptors are important regulators of cytokine production in non-pregnant mice, the alpha(2)- and the beta-adrenoceptor-mediated modulation of cytokine production ceases to operate during pregnancy associated with severe endotoxemia. These data may explain how excessive activation of the non-specific immune responses during pregnancy can contribute to the increased severity of some maternal diseases, including septic shock, and can be an important pathophysiological factor in disseminated intravascular coagulation or preeclampsia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-0795
pubmed:author
pubmed:issnType
Print
pubmed:volume
171
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
355-61
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11691656-Adrenergic alpha-Antagonists, pubmed-meshheading:11691656-Adrenergic beta-Antagonists, pubmed-meshheading:11691656-Animals, pubmed-meshheading:11691656-Berberine, pubmed-meshheading:11691656-Female, pubmed-meshheading:11691656-Gestational Age, pubmed-meshheading:11691656-Interferon-gamma, pubmed-meshheading:11691656-Interleukin-1, pubmed-meshheading:11691656-Interleukin-10, pubmed-meshheading:11691656-Interleukin-6, pubmed-meshheading:11691656-Lipopolysaccharides, pubmed-meshheading:11691656-Mice, pubmed-meshheading:11691656-Mice, Inbred Strains, pubmed-meshheading:11691656-Models, Animal, pubmed-meshheading:11691656-Pregnancy, pubmed-meshheading:11691656-Pregnancy Complications, Infectious, pubmed-meshheading:11691656-Propranolol, pubmed-meshheading:11691656-Shock, Septic, pubmed-meshheading:11691656-Tumor Necrosis Factor-alpha
pubmed:year
2001
pubmed:articleTitle
Enhanced tumor necrosis factor-alpha-specific and decreased interleukin-10-specific immune responses to LPS during the third trimester of pregnancy in mice.
pubmed:affiliation
Department of Pharmacology, Institute of Experimental Medicine, Hungarian Academy of Sciences, H-1450 Budapest, POB 67, Hungary. esvizi@koki.hu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't