Source:http://linkedlifedata.com/resource/pubmed/id/15192652
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2004-6-11
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pubmed:abstractText |
Complement-mediated opsonization and phagocytosis of encapsulated serotype 5 Staphylococcus aureus are essential to host defense. We describe the effects of complement depletion and deficiencies of C4, C5, and complement receptors 1 and 2 on mouse survival after intravenous exposure to S aureus. Depletion of complement proteins in C57BL/6 mice with the use of cobra-venom factor decreased survival compared with that of controls after the induction of bacteremia with mucoid (90% mortality), encapsulated (73%), and unencapsulated (59%) S aureus strains. In this model complement is even more important in the control of infection with encapsulated S aureus (80% of clinical isolates) than in the control of infection by unencapsulated strains. C4-deficient mice demonstrated similar mortality from bacteremia caused by encapsulated S aureus compared with controls, suggesting that in the unimmunized animal the alternative complement pathway contributes more to control of bacteremia caused by encapsulated S aureus than the classical complement pathway or mannan-binding lectin pathway. C5-deficient mice (B10.D2-H2(d) H2-T18(c) Hc(0)/oSnJ) showed similar mortality when subjected to bacteremia caused by encapsulated S aureus compared with C5-sufficient (B10.D2-Hc(1) H2(d) H2-T18(c)/nSnJ) mice, suggesting that in this model the anaphylatoxin C5a and the late complement cascade are not critical to survival of bacteremia induced with the use of these strains. However, C5-deficient mice depleted of C3 with the use of cobra-venom factor had 60% decreased survival compared with untreated C5-deficient mice with bacteremia induced by encapsulated S aureus, suggesting that in this model C3 is more critical than C5 in controlling S aureus bacteremia. Complement receptor 1 (CD35) is the primary receptor for the opsonin C3b. Mice deficient in CD35/CD21 showed a 67% decrease in survival compared with normal mice, suggesting that CD35/CD21 is of major importance in the control of S aureus-induced bacteremia.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C4,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C5,
http://linkedlifedata.com/resource/pubmed/chemical/Complement System Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement 3b,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement 3d
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0022-2143
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
143
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
358-65
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:15192652-Animals,
pubmed-meshheading:15192652-Bacteremia,
pubmed-meshheading:15192652-Complement C3,
pubmed-meshheading:15192652-Complement C4,
pubmed-meshheading:15192652-Complement C5,
pubmed-meshheading:15192652-Complement System Proteins,
pubmed-meshheading:15192652-Female,
pubmed-meshheading:15192652-Mice,
pubmed-meshheading:15192652-Mice, Congenic,
pubmed-meshheading:15192652-Mice, Inbred C57BL,
pubmed-meshheading:15192652-Mice, Knockout,
pubmed-meshheading:15192652-Receptors, Complement,
pubmed-meshheading:15192652-Receptors, Complement 3b,
pubmed-meshheading:15192652-Receptors, Complement 3d,
pubmed-meshheading:15192652-Staphylococcal Infections,
pubmed-meshheading:15192652-Staphylococcus aureus
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pubmed:year |
2004
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pubmed:articleTitle |
Role of complement receptors 1 and 2 (CD35 and CD21), C3, C4, and C5 in survival by mice of Staphylococcus aureus bacteremia.
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pubmed:affiliation |
Department of Pediatrics and Duke Clinical Research Institue, Duke University Medical Center, Durham, NC, USA. cunniok@chkd.org
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pubmed:publicationType |
Journal Article
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