IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Garyu, J. W. A.
Right arrow Articles by Dumler, J. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Garyu, J. W. A.
Right arrow Articles by Dumler, J. S.

 Previous Article  |  Next Article 

Infection and Immunity, February 2005, p. 1187-1190, Vol. 73, No. 2
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.2.1187-1190.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Defective Phagocytosis in Anaplasma phagocytophilum- Infected Neutrophils

Justin W. A. Garyu,1 Kyoung-seong Choi,1 Dennis J. Grab,2 and J. Stephen Dumler1*

Division of Medical Microbiology, Department of Pathology,1 Division of Infectious Diseases, Department of Pediatrics, The Johns Hopkins University School of Medicine, Baltimore, Maryland2

Received 1 September 2004/ Returned for modification 13 October 2004/ Accepted 19 October 2004

Anaplasma phagocytophilum infection induces functional neutrophil changes. Using both Candida albicans and fluorescent-aggregate phagocytosis assays, we examined whether neutrophil and dimethyl sulfoxide-differentiated HL-60 cell infection impairs internalization. A. phagocytophilum infection significantly decreased phagocytosis compared to that of controls (P < 0.05). This further impairment of neutrophil function may promote opportunistic infections and exacerbate disease.


* Corresponding author. Mailing address: Department of Pathology, Division of Medical Microbiology, The Johns Hopkins University School of Medicine, 720 Rutland Ave., Ross 624, Baltimore, MD 21205. Phone: (410) 955-8654. Fax: (443) 287-3665. E-mail: sdumler{at}jhmi.edu.

Editor: W. A. Petri, Jr.


Infection and Immunity, February 2005, p. 1187-1190, Vol. 73, No. 2
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.2.1187-1190.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2005 by the American Society for Microbiology. All rights reserved.