rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2001-1-29
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pubmed:abstractText |
The polymorphonuclear neutrophils (PMNs) of patients infected with human immunodeficiency virus type 1 (HIV-1) show impaired microbicidal responses. The present study assessed the functional integrity of PMN degranulation responses and the expression of specific receptors that mediate these responses in a group of children vertically infected with HIV-1. PMN degranulation in response to interleukin-8 (IL-8) and complement 5a (C5a) was measured in a group of HIV-1-infected children with mild and severe clinical disease and in an uninfected control group. In addition, the expression of CXCR1, CXCR2, and CD88 on whole-blood PMNs was quantified by flow cytometry. Although CXCR1 expression was found to be largely unaltered in the HIV-1-infected children relative to that in the control children, the intensity of CXCR2 expression was significantly reduced in those with severe disease. Furthermore, there was a significant reduction in the percentage of cells expressing CD88 and in the intensity of CD88 fluorescence in the HIV-1-infected children compared to that in control children, with CD88 fluorescence intensity more significantly reduced in the presence of severe disease. PMNs from a large proportion of the HIV-1-infected children either showed reciprocal degranulation responses or were unresponsive to IL-8 and C5a, whereas the PMNs from the uninfected children showed positive responses. Inefficient agonist-induced degranulation may contribute to the increased susceptibility of HIV-1-infected children to secondary microbial infections. Furthermore, reduced expression of CXCR2 and CD88 may be suggestive of defects in other functions of PMNs from HIV-1-infected children.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-10024568,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-10225834,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-10515814,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-1500735,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-1840701,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-1856598,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-211165,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-2170609,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-2257291,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-2491503,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-2824608,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-2842409,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-2842543,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-4473046,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-4825785,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-6088649,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11139191-9952364
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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/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C5a,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Anaphylatoxin C5a,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-8A,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-8B
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1071-412X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
21-30
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:11139191-Age Factors,
pubmed-meshheading:11139191-Antigens, CD,
pubmed-meshheading:11139191-CD4 Lymphocyte Count,
pubmed-meshheading:11139191-Cell Degranulation,
pubmed-meshheading:11139191-Child,
pubmed-meshheading:11139191-Child, Preschool,
pubmed-meshheading:11139191-Complement C5a,
pubmed-meshheading:11139191-Down-Regulation,
pubmed-meshheading:11139191-HIV Infections,
pubmed-meshheading:11139191-HIV-1,
pubmed-meshheading:11139191-Humans,
pubmed-meshheading:11139191-Infant,
pubmed-meshheading:11139191-Infectious Disease Transmission, Vertical,
pubmed-meshheading:11139191-Interleukin-8,
pubmed-meshheading:11139191-Neutrophils,
pubmed-meshheading:11139191-Receptor, Anaphylatoxin C5a,
pubmed-meshheading:11139191-Receptors, Complement,
pubmed-meshheading:11139191-Receptors, Interleukin-8A,
pubmed-meshheading:11139191-Receptors, Interleukin-8B
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pubmed:year |
2001
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pubmed:articleTitle |
Defective neutrophil degranulation induced by interleukin-8 and complement 5a and down-regulation of associated receptors in children vertically infected with human immunodeficiency virus type 1.
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pubmed:affiliation |
AIDS Virus Research Unit, National Institute for Virology, Johannesburg, South Africa.
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pubmed:publicationType |
Journal Article
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