Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-8-24
pubmed:abstractText
While the effects of interleukin-3 (IL-3) and granulocyte macrophage-colony stimulating factor (GM-CSF) on microglia are well documented, very little is known about the effects of a related cytokine, interleukin-5 (IL-5). We therefore undertook studies to determine how IL-5 alters various aspects of microglial functioning. Treatment of microglia with IL-5 resulted in the induction of proliferation at levels similar to those induced by GM-CSF. IL-5 also increased cellular metabolism of microglial cells. To determine whether increased metabolism correlated with activation of microglia, we measured levels of nitrite, a breakdown product of nitric oxide. Treatment of microglial cultures with IL-5 increased nitrite levels, while GM-CSF treatment had no effect. Treatment of microglia with IL-5 did not cause activation of the signal transduction pathways linked to the classical IL-5 receptor, STAT5A/5B and ERK1 and ERK2. It is therefore likely that the effects of IL-5 on microglia are not mediated via the classical IL-5 receptor, but rather via a novel receptor.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0364-3190
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
629-37
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
IL-5 induces proliferation and activation of microglia via an unknown receptor.
pubmed:affiliation
Department of Neurobiology, Mental Retardation Research Center, Brain Research Institute, UCLA School of Medicine, Los Angeles, California 90095, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.