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 Kielian, T.
Right arrow Articles by Esen, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kielian, T.
Right arrow Articles by Esen, N.

 Previous Article  |  Next Article 

Infection and Immunity, November 2005, p. 7428-7435, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7428-7435.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Toll-Like Receptor 2 Modulates the Proinflammatory Milieu in Staphylococcus aureus-Induced Brain Abscess

Tammy Kielian,* Anessa Haney, Patrick M. Mayes, Sarita Garg, and Nilufer Esen

Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205

Received 21 June 2005/ Returned for modification 19 July 2005/ Accepted 16 August 2005

Toll-like receptor 2 (TLR2) is a pattern recognition receptor (PRR) that plays an important role in innate immune recognition of conserved structural motifs on a wide array of pathogens, including Staphylococcus aureus. To ascertain the functional significance of TLR2 in the context of central nervous system (CNS) parenchymal infection, we evaluated the pathogenesis of S. aureus-induced experimental brain abscess in TLR2 knockout (KO) and wild-type (WT) mice. The expression of several proinflammatory mediators, including inducible nitric oxide synthase, tumor necrosis factor alpha, and macrophage inflammatory protein-2, was significantly attenuated in brain abscesses of TLR2 KO mice compared to WT mice during the acute phase of infection. Conversely, interleukin-17 (IL-17), a cytokine produced by activated and memory T cells, was significantly elevated in lesions of TLR2 KO mice, suggesting an association between innate and adaptive immunity in brain abscess. Despite these differences, brain abscess severity in TLR2 KO and WT animals was similar, with comparable mortality rates, bacterial titers, and blood-brain barrier permeability, implying a role for alternative PRRs. Expression of the phagocytic PRRs macrophage scavenger receptor type AI/AII and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) was increased in brain abscesses of both TLR2 KO and WT mice compared to uninfected animals. However, LOX-1 induction in brain abscesses of TLR2 KO mice was significantly attenuated compared to WT animals, revealing that the TLR2-dependent signal(s) influence LOX-1 expression. Collectively, these findings reveal the complex nature of gram-positive bacterial recognition in the CNS which occurs, in part, through engagement of TLR2 and highlight the importance of receptor redundancy for S. aureus detection in the CNS.

* Corresponding author. Mailing address: Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, 4301 W. Markham St., Slot 846, Little Rock, AR 72205. Phone: (501) 526-6348. Fax: (501) 526-6756. E-mail: KielianTammyL{at}uams.edu.

Editor: J. D. Clements

Infection and Immunity, November 2005, p. 7428-7435, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7428-7435.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Nichols, J. R., Aldrich, A. L., Mariani, M. M., Vidlak, D., Esen, N., Kielian, T. (2009). TLR2 Deficiency Leads to Increased Th17 Infiltrates in Experimental Brain Abscesses. J. Immunol. 182: 7119-7130 [Abstract] [Full Text]  
  • Yoon, H. J., Jeon, S.-B., Kim, I.-H., Park, E. J. (2008). Regulation of TLR2 Expression by Prostaglandins in Brain Glia. J. Immunol. 180: 8400-8409 [Abstract] [Full Text]  
  • Kielian, T., Syed, M. Md., Liu, S., Phulwani, N. K., Phillips, N., Wagoner, G., Drew, P. D., Esen, N. (2008). The Synthetic Peroxisome Proliferator-Activated Receptor-{gamma} Agonist Ciglitazone Attenuates Neuroinflammation and Accelerates Encapsulation in Bacterial Brain Abscesses. J. Immunol. 180: 5004-5016 [Abstract] [Full Text]  
  • Stenzel, W., Soltek, S., Sanchez-Ruiz, M., Akira, S., Miletic, H., Schluter, D., Deckert, M. (2008). Both TLR2 and TLR4 Are Required for the Effective Immune Response in Staphylococcus aureus-Induced Experimental Murine Brain Abscess. Am. J. Pathol. 172: 132-145 [Abstract] [Full Text]  
  • Kielian, T., Esen, N., Liu, S., Phulwani, N. K., Syed, M. M., Phillips, N., Nishina, K., Cheung, A. L., Schwartzman, J. D., Ruhe, J. J. (2007). Minocycline Modulates Neuroinflammation Independently of Its Antimicrobial Activity in Staphylococcus aureus-Induced Brain Abscess. Am. J. Pathol. 171: 1199-1214 [Abstract] [Full Text]  
  • Kielian, T., Phulwani, N. K., Esen, N., Syed, M. Md., Haney, A. C., McCastlain, K., Johnson, J. (2007). MyD88-Dependent Signals Are Essential for the Host Immune Response in Experimental Brain Abscess. J. Immunol. 178: 4528-4537 [Abstract] [Full Text]  
  • Chen, K., Iribarren, P., Hu, J., Chen, J., Gong, W., Cho, E. H., Lockett, S., Dunlop, N. M., Wang, J. M. (2006). Activation of Toll-like Receptor 2 on Microglia Promotes Cell Uptake of Alzheimer Disease-associated Amyloid beta Peptide. J. Biol. Chem. 281: 3651-3659 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»