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 Sun, Y.-H.
Right arrow Articles by Tsolis, R. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sun, Y.-H.
Right arrow Articles by Tsolis, R. M.

 Previous Article  |  Next Article 

Infection and Immunity, September 2002, p. 4826-4832, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.4826-4832.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

virB-Mediated Survival of Brucella abortus in Mice and Macrophages Is Independent of a Functional Inducible Nitric Oxide Synthase or NADPH Oxidase in Macrophages

Yao-Hui Sun,1 Andreas B. den Hartigh,1 Renato de Lima Santos,2 L. Garry Adams,3 and Renée M. Tsolis1*

Department of Medical Microbiology and Immunology, Texas A&M University System Health Science Center,1 Veterinary Pathobiology, Texas A&M University, College Station, Texas,3 Universidade Federal de Minas Gerais, Belo Horizonte, Brazil2

Received 19 April 2002/ Returned for modification 28 May 2002/ Accepted 6 June 2002

The Brucella abortus virB locus is required for establishing chronic infection in the mouse. Using in vitro and in vivo models, we investigated whether virB is involved in evasion of the bactericidal activity of NADPH oxidase and the inducible nitric oxide synthase (iNOS) in macrophages. Elimination of NADPH oxidase or iNOS activity in macrophages in vitro increased recovery of wild-type B. abortus but not recovery of a virB mutant. In mice lacking either NADPH oxidase or iNOS, however, B. abortus infected and persisted to the same extent as it did in congenic C57BL/6 mice up until 60 days postinfection, suggesting that these host defense mechanisms are not critical for limiting bacterial growth in the mouse. A virB mutant did not exhibit increased survival in either of the knockout mouse strains, indicating that this locus does not contribute to evasion of nitrosative or oxidative killing mechanisms in vivo.


* Corresponding author. Mailing address: Department of Medical Microbiology, 407 Reynolds Medical Building, College Station, TX 77843-1114. Phone: (979) 845-1314. Fax: (979) 845-3479. E-mail: rtsolis{at}medicine.tamu.edu.

Editor: D. L. Burns


Infection and Immunity, September 2002, p. 4826-4832, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.4826-4832.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Lahiri, A., Das, P., Chakravortty, D. (2008). The LysR-type transcriptional regulator Hrg counteracts phagocyte oxidative burst and imparts survival advantage to Salmonella enterica serovar Typhimurium. Microbiology 154: 2837-2846 [Abstract] [Full Text]  
  • Rolan, H. G., Tsolis, R. M. (2008). Inactivation of the Type IV Secretion System Reduces the Th1 Polarization of the Immune Response to Brucella abortus Infection. Infect. Immun. 76: 3207-3213 [Abstract] [Full Text]  
  • Rolan, H. G., den Hartigh, A. B., Kahl-McDonagh, M., Ficht, T., Adams, L. G., Tsolis, R. M. (2008). VirB12 Is a Serological Marker of Brucella Infection in Experimental and Natural Hosts. CVI 15: 208-214 [Abstract] [Full Text]  
  • Rolan, H. G., Tsolis, R. M. (2007). Mice Lacking Components of Adaptive Immunity Show Increased Brucella abortus virB Mutant Colonization. Infect. Immun. 75: 2965-2973 [Abstract] [Full Text]  
  • Sun, Y.-H., Rolan, H. G., den Hartigh, A. B., Sondervan, D., Tsolis, R. M. (2005). Brucella abortus VirB12 Is Expressed during Infection but Is Not an Essential Component of the Type IV Secretion System. Infect. Immun. 73: 6048-6054 [Abstract] [Full Text]  
  • den Hartigh, A. B., Sun, Y.-H., Sondervan, D., Heuvelmans, N., Reinders, M. O., Ficht, T. A., Tsolis, R. M. (2004). Differential Requirements for VirB1 and VirB2 during Brucella abortus Infection. Infect. Immun. 72: 5143-5149 [Abstract] [Full Text]  
  • Celli, J., de Chastellier, C., Franchini, D.-M., Pizarro-Cerda, J., Moreno, E., Gorvel, J.-P. (2003). Brucella Evades Macrophage Killing via VirB-dependent Sustained Interactions with the Endoplasmic Reticulum. JEM 198: 545-556 [Abstract] [Full Text]  
  • Aguzzi, A., Hardt, W.-D. (2003). Dangerous Liaisons between a Microbe and the Prion Protein. JEM 198: 1-4 [Full Text]  
  • Watarai, M., Kim, S., Erdenebaatar, J., Makino, S.-i., Horiuchi, M., Shirahata, T., Sakaguchi, S., Katamine, S. (2003). Cellular Prion Protein Promotes Brucella Infection into Macrophages. JEM 198: 5-17 [Abstract] [Full Text]