Source:http://linkedlifedata.com/resource/pubmed/id/18390928
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2008-7-2
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pubmed:abstractText |
In the present study, we investigated whether saliva from Phlebotomus papatasi and Phlebotomus duboscqi inhibited antigen-induced neutrophil migration and the mechanisms involved in these effects. The pretreatment of immunized mice with salivary gland extracts (SGE) of both phlebotomines inhibited OVA challenge-induced neutrophil migration and release of the neutrophil chemotactic mediators, MIP-1alpha, TNF-alpha, and leukotriene B4 (LTB4). Furthermore, SGE treatment enhanced the production of anti-inflammatory mediators, IL-10 and PGE2. SGE treatments failed to inhibit neutrophil migration and MIP-1alpha and LTB4 production in IL-10-/- mice, also failing in mice treated with nonselective (indomethacin) or selective (rofecoxibe) cyclooxygenase (COX) inhibitors. COX inhibition resulted in diminished SGE-induced IL-10 production, and PGE2 release triggered by SGE remained increased in IL-10-/- mice, suggesting that prostanoids are acting through an IL-10-dependent mechanism. SGE treatments in vivo reduced the OVA-induced lymphoproliferation of spleen-derived cells. Further, the in vitro incubation of bone marrow-derived dendritic cells (DC) with SGE inhibited the proliferation of CD4+T cells from OVA-immunized mice, which was reversed by indomethacin and anti-IL-10 antibody treatments. Supporting these results, SGE induced the production of PGE2 and IL-10 by DC, which were blocked by COX inhibition. These effects were associated with the reduction of DC-membrane expression of MHC-II and CD86 by SGE treatment. Altogether, the results showed that Phlebotomine saliva inhibits immune inflammation-induced neutrophil migration by an autocrine DC sequential production of PGE2/IL-10, suggesting that the saliva constituents might be promising therapeutic molecules to target immune inflammatory diseases.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin,
http://linkedlifedata.com/resource/pubmed/chemical/Tissue Extracts
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0741-5400
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pubmed:author |
pubmed-author:CarregaroVanessaV,
pubmed-author:CunhaFernando QFQ,
pubmed-author:CunhaThiago MTM,
pubmed-author:ElnaiemDia-EldinDE,
pubmed-author:GrespanRenataR,
pubmed-author:MatsumuraGrazielaG,
pubmed-author:RibeiroJosé M CJM,
pubmed-author:SilvaJoão SJS,
pubmed-author:ValenzuelaJesus GJG,
pubmed-author:VerriWaldiceu AWAJr
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pubmed:issnType |
Print
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pubmed:volume |
84
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
104-14
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pubmed:dateRevised |
2011-10-4
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pubmed:meshHeading |
pubmed-meshheading:18390928-Animals,
pubmed-meshheading:18390928-Antigen Presentation,
pubmed-meshheading:18390928-Autocrine Communication,
pubmed-meshheading:18390928-Cell Movement,
pubmed-meshheading:18390928-Chemotaxis,
pubmed-meshheading:18390928-Dendritic Cells,
pubmed-meshheading:18390928-Dinoprostone,
pubmed-meshheading:18390928-Female,
pubmed-meshheading:18390928-Inflammation,
pubmed-meshheading:18390928-Interleukin-10,
pubmed-meshheading:18390928-Lipopolysaccharides,
pubmed-meshheading:18390928-Mice,
pubmed-meshheading:18390928-Neutrophils,
pubmed-meshheading:18390928-Ovalbumin,
pubmed-meshheading:18390928-Peritonitis,
pubmed-meshheading:18390928-Phlebotomus,
pubmed-meshheading:18390928-Saliva,
pubmed-meshheading:18390928-Tissue Extracts
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pubmed:year |
2008
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pubmed:articleTitle |
Phlebotomine salivas inhibit immune inflammation-induced neutrophil migration via an autocrine DC-derived PGE2/IL-10 sequential pathway.
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pubmed:affiliation |
Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of Sao Paulo, Av Bandeirantes, 3900, Ribeirão Preto, SP, Brazil, 14049-900.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Intramural
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