Source:http://linkedlifedata.com/resource/pubmed/id/12480703
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
8
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| pubmed:dateCreated |
2003-4-3
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| pubmed:abstractText |
Tick saliva contains anti-inflammatory and immunosuppressive substances that facilitate blood feeding and enhance tick-vectored pathogen transmission, including Anaplasma phagocytophila an etiologic agent of granulocytic ehrlichiosis. As such, inflammation at a tick-feeding site is strikingly different than that typically observed at other sites of inflammation. Up-regulation of CD11b/CD18 occurs in host granulocytes following interaction or infection with A phagocytophila, and the absence of CD11b/CD18 results in early increases in bacteremia. We hypothesized that beta 2 integrin-dependent infection kinetics and leukocyte extravasation are important determinants of neutrophil trafficking to, and pathogen acquisition at, tick-feeding sites. A phagocytophila infection kinetics were evaluated in CD11a/CD18, CD11b/CD18, and CD18 knock-out mice using quantitative polymerase chain reaction (PCR) of blood, ticks, and skin biopsies in conjunction with histopathology. A marked increase in the rate of A phagocytophila infection of neutrophils and pathogen burden in blood followed tick feeding. Infection kinetics were modified by beta 2 integrin expression and systemic neutrophil counts. Significant neutrophil-pathogen trafficking was observed to both suture and tick sites. Despite the prominent role for beta 2 integrins in neutrophil arrest in flowing blood, successful pathogen acquisition by ticks occurred in the absence of beta 2 integrins. Establishment of feeding pools that rely less on leukocyte trafficking and more on small hemorrhages may explain the ready amplification of A phagocytophila DNA from ticks infested on CD11/CD18-deficient mouse strains.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
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| pubmed:issn |
0006-4971
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
15
|
| pubmed:volume |
101
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3257-64
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:12480703-Anaplasma phagocytophilum,
pubmed-meshheading:12480703-Animals,
pubmed-meshheading:12480703-Antigens, CD11a,
pubmed-meshheading:12480703-Antigens, CD11b,
pubmed-meshheading:12480703-Antigens, CD18,
pubmed-meshheading:12480703-Arachnid Vectors,
pubmed-meshheading:12480703-Bacteremia,
pubmed-meshheading:12480703-Chemotaxis, Leukocyte,
pubmed-meshheading:12480703-Ehrlichiosis,
pubmed-meshheading:12480703-Female,
pubmed-meshheading:12480703-Foreign-Body Reaction,
pubmed-meshheading:12480703-Hemorrhage,
pubmed-meshheading:12480703-Humans,
pubmed-meshheading:12480703-Inflammation,
pubmed-meshheading:12480703-Ixodes,
pubmed-meshheading:12480703-Kinetics,
pubmed-meshheading:12480703-Leukocyte Count,
pubmed-meshheading:12480703-Mice,
pubmed-meshheading:12480703-Mice, Inbred C3H,
pubmed-meshheading:12480703-Mice, Knockout,
pubmed-meshheading:12480703-Mice, SCID,
pubmed-meshheading:12480703-Neutrophils,
pubmed-meshheading:12480703-Skin,
pubmed-meshheading:12480703-Specific Pathogen-Free Organisms,
pubmed-meshheading:12480703-Sutures,
pubmed-meshheading:12480703-Tick Infestations
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| pubmed:year |
2003
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| pubmed:articleTitle |
Roles of neutrophil beta 2 integrins in kinetics of bacteremia, extravasation, and tick acquisition of Anaplasma phagocytophila in mice.
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| pubmed:affiliation |
Center for Comparative Medicine, Schools of Medicine Veterinary Medicine, University of California, Davis 95616, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|