Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1996-11-7
pubmed:abstractText
Vitamin A deficiency predisposes the host for a strong inflammatory response, suggesting that it may foster susceptibility to diseases, such as Lyme arthritis, in which activated macrophage and inflammatory cytokine production are pathogenic. Infected mice had a rapid serum retinal decline that correlated with the onset of arthritis. The mice with the least retinol developed acute arthritis earlier and more severely than those with the highest retinol. Earlier and stronger interleukin (IL)-12, interferon-gamma (IFN)-gamma, and tumor necrosis factor responses were found in Borrelia burgdorferi-infected, vitamin A-deficient mice compared with controls. The spirochetes induced IFN-gamma secretion from unprimed cells, and retinoid addition in vitro inhibited IFN-gamma synthesis. Vitamin A deficiency may exacerbate acute Lyme arthritis by enhancing an acute arthritogenic inflammatory response initiated by spirochete-driven IFN-gamma secretion. Conversely, vitamin A may lessen acute Lyme arthritis pathology by blocking IFN-gamma and IL-12 synthesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1899
pubmed:author
pubmed:issnType
Print
pubmed:volume
174
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
747-51
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Vitamin A deficiency exacerbates murine Lyme arthritis.
pubmed:affiliation
Department of Biochemistry, University of Wisconsin-Madison 53706, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.