|
|
Prepublished online as a Blood First Edition Paper on December 12, 2002; DOI 10.1182/blood-2002-04-1019.
 Previous Article | Table of Contents | Next Article 
Blood, 15 April 2003, Vol. 101, No. 8, pp. 3257-3264
PHAGOCYTES
Roles of neutrophil  2 integrins in kinetics of bacteremia,
extravasation, and tick acquisition of Anaplasma
phagocytophila in mice
Dori L. Borjesson,
Scott I. Simon,
Emir Hodzic,
Hilde E. V. DeCock,
Christie M. Ballantyne, and
Stephen W. Barthold
From the Center for Comparative Medicine, Schools of
Medicine and Veterinary Medicine; Department of Biomedical Engineering;
and Department of Veterinary Medicine: Pathology, Microbiology and
Immunology, University of California, Davis; and Section of
Atherosclerosis and Leukocyte Biology, Departments of Medicine and
Pediatrics, Baylor College of Medicine, Houston, TX.
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
 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 2 integrin expression and systemic neutrophil counts. Significant
neutrophil-pathogen trafficking was observed to both suture and tick
sites. Despite the prominent role for 2 integrins in neutrophil
arrest in flowing blood, successful pathogen acquisition by ticks
occurred in the absence of 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.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
U. Blas-Machado, J. de la Fuente, E. F. Blouin, C. Almazan, K. M. Kocan, and J. V. Mysore
Experimental Infection of C3H/HeJ Mice with the NY18 Isolate of Anaplasma phagocytophilum
Vet. Pathol.,
January 1, 2007;
44(1):
64 - 73.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. L. Borjesson, S. D. Kobayashi, A. R. Whitney, J. M. Voyich, C. M. Argue, and F. R. DeLeo
Insights into Pathogen Immune Evasion Mechanisms: Anaplasma phagocytophilum Fails to Induce an Apoptosis Differentiation Program in Human Neutrophils
J. Immunol.,
May 15, 2005;
174(10):
6364 - 6372.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. T. Brandhorst, M. Wuthrich, B. Finkel-Jimenez, T. Warner, and B. S. Klein
Exploiting Type 3 Complement Receptor for TNF-{alpha} Suppression, Immune Evasion, and Progressive Pulmonary Fungal Infection
J. Immunol.,
December 15, 2004;
173(12):
7444 - 7453.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Wu, J. R. Rodgers, X.-Y. D. Perrard, J. L. Perrard, J. E. Prince, Y. Abe, B. K. Davis, G. Dietsch, C. W. Smith, and C. M. Ballantyne
Deficiency of CD11b or CD11d Results in Reduced Staphylococcal Enterotoxin-Induced T Cell Response and T Cell Phenotypic Changes
J. Immunol.,
July 1, 2004;
173(1):
297 - 306.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. D. van Buul and P. L. Hordijk
Signaling in Leukocyte Transendothelial Migration
Arterioscler. Thromb. Vasc. Biol.,
May 1, 2004;
24(5):
824 - 833.
[Abstract]
[Full Text]
|
|
|
| |
