Linked Life Data

18354219

Source:http://linkedlifedata.com/resource/pubmed/id/18354219

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2008-3-20
pubmed:abstractText
We recently demonstrated that in vitro peroxisome proliferator-activated receptor-gamma (PPARgamma) activation of mouse peritoneal macrophages by IL-13 or PPARgamma ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2(-/-)) mice with natural and synthetic PPARgamma-specific ligands or with IL-13 decreases C. albicans colonization of the gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARgamma antagonist, and are reduced in PPARgamma(+/-) mice. Overall, these data demonstrate that IL-13 or PPARgamma ligands attenuate C. albicans infection of the GI tract through PPARgamma activation and hence suggest that PPARgamma ligands may be of therapeutic value in esophageal and GI candidiasis in immunocompromised patients.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
180
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4939-47
pubmed:meshHeading
pubmed-meshheading:18354219-Animals, pubmed-meshheading:18354219-Candida albicans, pubmed-meshheading:18354219-Candidiasis, pubmed-meshheading:18354219-Cecum, pubmed-meshheading:18354219-Cell Movement, pubmed-meshheading:18354219-DNA-Binding Proteins, pubmed-meshheading:18354219-Female, pubmed-meshheading:18354219-Gastrointestinal Diseases, pubmed-meshheading:18354219-Immunologic Deficiency Syndromes, pubmed-meshheading:18354219-Interleukin-13, pubmed-meshheading:18354219-Lectins, C-Type, pubmed-meshheading:18354219-Ligands, pubmed-meshheading:18354219-Macrophages, pubmed-meshheading:18354219-Mannose-Binding Lectins, pubmed-meshheading:18354219-Mice, pubmed-meshheading:18354219-Mice, Knockout, pubmed-meshheading:18354219-PPAR gamma, pubmed-meshheading:18354219-Receptors, Cell Surface, pubmed-meshheading:18354219-Thiazolidinediones
pubmed:year
2008
pubmed:articleTitle
IL-13 attenuates gastrointestinal candidiasis in normal and immunodeficient RAG-2(-/-) mice via peroxisome proliferator-activated receptor-gamma activation.
pubmed:affiliation
Laboratoire Polarisation des Macrophages and Récepteurs Nucléaires dans les Pathologies Inflammatoires et Infectieuses, Université Paul Sabatier Toulouse III, INSERM, Institut Fédératif de Recherche 31, Institut Louis Bugnard, Toulouse, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't