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 Cao, F.
Right arrow Articles by Byrne, G. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cao, F.
Right arrow Articles by Byrne, G. I.

 Previous Article  |  Next Article 

Infection and Immunity, February 2007, p. 753-759, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.01386-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Chlamydia pneumoniae-Induced Macrophage Foam Cell Formation Is Mediated by Toll-Like Receptor 2{triangledown}

Fei Cao,1 Antonio Castrillo,2,{dagger} Peter Tontonoz,2 Fabio Re,1 and Gerald I. Byrne1*

Department of Molecular Sciences, University of Tennessee Health Science Center, Memphis, Tennessee,1 Howard Hughes Medical Institute and Department of Pathology and Laboratory Medicine, University of California, Los Angeles, Los Angeles, California2

Received 29 August 2006/ Returned for modification 2 November 2006/ Accepted 22 November 2006

Chlamydia pneumoniae induces macrophage foam cell formation, a hallmark of early atherosclerosis, in the presence of low-density lipoprotein (LDL). This study examined the role that Toll-like receptor 2 (TLR2) and TLR4 may play in pathogen-induced foam cell formation. Murine macrophage RAW 264.7 cells either infected with C. pneumoniae or treated with the TLR4 ligand E. coli lipopolysaccharide (LPS) or the TLR2 ligand Pam3-Cys-Ala-Gly-OH (Pam) became Oil Red O-stained foam cells and showed increased cholesteryl ester (CE) content when cocultured with LDL. In macrophages from TLR2–/– mice, foam cells were induced by Escherichia coli LPS but not by C. pneumoniae or Pam. Conversely, C. pneumoniae or Pam, but not E. coli LPS, induced foam cells in the TLR4-deficient GG2EE macrophage cell line, suggesting that C. pneumoniae elicits foam cell formation predominantly via TLR2. Enhancing cholesterol efflux using the liver X receptor (LXR) agonist GW3965 significantly decreased the CE content of cells exposed to each of the three TLR ligands (C. pneumoniae, Pam, and E. coli LPS). Overall, our results suggest that activation of the LXR signaling pathway may affect potentially atherogenic processes modulated by the TLR ligands.

* Corresponding author. Mailing address: Department of Molecular Sciences, University of Tennessee Health Science Center, 858 Madison Ave., Memphis, TN 38163. Phone: (901) 488-6150. Fax: (901) 488-3330. E-mail: gbyrne{at}utmem.edu.

{triangledown} Published ahead of print on 4 December 2006.

Editor: J. N. Weiser

{dagger} Present address: Departmento Bioquimicay, Biologia Molecular, Universidad Las Palmas Gran Canaria, Las Palmas, Spain.

Infection and Immunity, February 2007, p. 753-759, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.01386-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Almeida, P. E., Silva, A. R., Maya-Monteiro, C. M., Torocsik, D., D'Avila, H., Dezso, B., Magalhaes, K. G., Castro-Faria-Neto, H. C., Nagy, L., Bozza, P. T. (2009). Mycobacterium bovis Bacillus Calmette-Guerin Infection Induces TLR2-Dependent Peroxisome Proliferator-Activated Receptor {gamma} Expression and Activation: Functions in Inflammation, Lipid Metabolism, and Pathogenesis. J. Immunol. 183: 1337-1345 [Abstract] [Full Text]  
  • Naiki, Y., Sorrentino, R., Wong, M. H., Michelsen, K. S., Shimada, K., Chen, S., Yilmaz, A., Slepenkin, A., Schroder, N. W. J., Crother, T. R., Bulut, Y., Doherty, T. M., Bradley, M., Shaposhnik, Z., Peterson, E. M., Tontonoz, P., Shah, P. K., Arditi, M. (2008). TLR/MyD88 and Liver X Receptor {alpha} Signaling Pathways Reciprocally Control Chlamydia pneumoniae-Induced Acceleration of Atherosclerosis. J. Immunol. 181: 7176-7185 [Abstract] [Full Text]  
  • Chen, S., Sorrentino, R., Shimada, K., Bulut, Y., Doherty, T. M., Crother, T. R., Arditi, M. (2008). Chlamydia pneumoniae-Induced Foam Cell Formation Requires MyD88-Dependent and -Independent Signaling and Is Reciprocally Modulated by Liver X Receptor Activation. J. Immunol. 181: 7186-7193 [Abstract] [Full Text]  
  • Pacheco, P., Vieira-de-Abreu, A., Gomes, R. N., Barbosa-Lima, G., Wermelinger, L. B., Maya-Monteiro, C. M., Silva, A. R., Bozza, M. T., Castro-Faria-Neto, H. C., Bandeira-Melo, C., Bozza, P. T. (2007). Monocyte Chemoattractant Protein-1/CC Chemokine Ligand 2 Controls Microtubule-Driven Biogenesis and Leukotriene B4-Synthesizing Function of Macrophage Lipid Bodies Elicited by Innate Immune Response. J. Immunol. 179: 8500-8508 [Abstract] [Full Text]  
  • Niessner, A., Shin, M. S., Pryshchep, O., Goronzy, J. J., Chaikof, E. L., Weyand, C. M. (2007). Synergistic Proinflammatory Effects of the Antiviral Cytokine Interferon-{alpha} and Toll-Like Receptor 4 Ligands in the Atherosclerotic Plaque. Circulation 116: 2043-2052 [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»