Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-5-30
pubmed:abstractText
Interleukin-1 beta (IL-1 beta) has been shown by several investigators to be a stimulator of adrenal glucocorticoid production in vivo. However, little evidence exists for direct actions of IL-1 beta on the adrenal gland. We sought to elucidate the direct effects, if any, of IL-1 beta on human fetal adrenal steroidogenesis in the presence and absence of ACTH in both cell and organ cultures. We studied the effects of several doses of recombinant human IL-1 beta (0.05, 0.5, and 5 U/ml), in the presence and absence of two doses of ACTH (0.1 and 1 microgram/ml). With all doses of IL-1 beta, we were unable to demonstrate alterations in basal adrenal steroidogenesis as measured by dehydroepiandrosterone sulfate and cortisol production. Whereas both doses of ACTH induced significant increases in steroid production over control values (P less than 0.05), there was no additional effect on steroidogenesis when IL-1 beta was added to cultures containing ACTH. We conclude that although IL-1 beta may act in conjunction with other products of the immune system to modulate adrenal cortisol production, IL-1 beta alone does not directly influence human fetal adrenal steroidogenesis. Rather, it is likely that this cytokine acts via stimulation of pituitary ACTH production.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0039-128X
pubmed:author
pubmed:issnType
Print
pubmed:volume
56
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
72-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Investigation of the effect of interleukin-1 beta on steroidogenesis in the human fetal adrenal gland.
pubmed:affiliation
Department of Obstetrics and Gynecology, University of Alabama, Birmingham 35294.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.