This Article Full Text (PDF) Other Versions of this Article: IAI.00868-06v1 74/12/6590    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rasmussen, J. W. Articles by Benach, J. L. Search for Related Content PubMed PubMed Citation Articles by Rasmussen, J. W. Articles by Benach, J. L.

 Previous Article  |  Next Article 

Infect. Immun. doi:10.1128/IAI.00868-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Mac-1⁺ cells are the predominant subset in the early hepatic lesions of mice infected with Francisella tularensis

Center for Infectious Diseases, Department of Pathology, and Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York 11794

^* To whom correspondence should be addressed. Email: jbenach{at}notes.cc.sunysb.edu.

	Abstract

The cell composition of early hepatic lesions of experimental murine tularemia has not been characterized with specific markers. The appearance of multiple granulomatous-necrotic lesions in the liver correlates with a marked increase in the levels of serum alanine transferase and lactate dehydrogenase. Francisella tularensis, detected by specific antibodies, can be first noted by day one and becomes associated with the lesions by five days post inoculation. These lesions become necrotic with some evidence of in situ apoptosis. The lesions do not contain B, T, or NK cells. Rather, the lesions are largely composed of two subpopulations of Mac-1⁺ cells that are associated with the bacteria. Gr-1⁺ Mac-1⁺ immature myeloid cells and MHC II⁺ Mac-1⁺ macrophages were the most abundant cell phenotypes found in the granuloma and are likely major contributors to control the infection in its early stages. Our findings have shown that there is an early development of hepatic lesions where F. tularensis colocalizes with both Gr-1⁺ Mac-1⁺ and MHC II⁺ Mac-1⁺ cells.

This article has been cited by other articles:

• Woolard, M. D., Hensley, L. L., Kawula, T. H., Frelinger, J. A. (2008). Respiratory Francisella tularensis Live Vaccine Strain Infection Induces Th17 Cells and Prostaglandin E2, Which Inhibits Generation of Gamma Interferon-Positive T Cells. Infect. Immun. 76: 2651-2659 [Abstract] [Full Text]  
• Bokhari, S. M., Kim, K.-J., Pinson, D. M., Slusser, J., Yeh, H.-W., Parmely, M. J. (2008). NK Cells and Gamma Interferon Coordinate the Formation and Function of Hepatic Granulomas in Mice Infected with the Francisella tularensis Live Vaccine Strain. Infect. Immun. 76: 1379-1389 [Abstract] [Full Text]  
• Lindemann, S. R., McLendon, M. K., Apicella, M. A., Jones, B. D. (2007). An In Vitro Model System Used To Study Adherence and Invasion of Francisella tularensis Live Vaccine Strain in Nonphagocytic Cells. Infect. Immun. 75: 3178-3182 [Abstract] [Full Text]