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 Al-Younes, H. M.
Right arrow Articles by Meyer, T. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Al-Younes, H. M.
Right arrow Articles by Meyer, T. F.

 Previous Article  |  Next Article 

Infection and Immunity, August 2004, p. 4751-4762, Vol. 72, No. 8
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.8.4751-4762.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Interaction of Chlamydia trachomatis Serovar L2 with the Host Autophagic Pathway

Hesham M. Al-Younes,1 Volker Brinkmann,2 and Thomas F. Meyer1*

Department of Molecular Biology,1 Central Microscopy Unit, Max Planck Institute for Infection Biology, D-10117 Berlin, Germany2

Received 20 January 2004/ Returned for modification 19 February 2004/ Accepted 23 April 2004

Chlamydiae are obligate intracellular pathogens that replicate within a membrane-bound compartment (the inclusion) and are associated with important human diseases, such as trachoma, pneumonia, and atherosclerosis. We have examined the interaction of the host autophagic pathway with Chlamydia trachomatis serovar L2 by using the specific autophagosomal stain monodansylcadaverine, antibodies to autophagosome-associated markers, and traditionally used autophagic inhibitors, particularly 3-methyladenine and amino acids. Chlamydial inclusions did not sequester monodansylcadaverine, suggesting absence of fusion with autophagosomes. Interestingly, exposure of cultures infected for 19 h to 3-methyladenine or single amino acids until the end of infection (44 h) caused various degrees of abnormalities in the inclusion maturation and in the progeny infectivity. Incubation of host cells with chemicals throughout the entire period of infection modulated the growth of Chlamydia even more dramatically. Remarkably, autophagosomal markers MAP-LC3 and calreticulin were redistributed to the inclusion of Chlamydia, a process that appears to be sensitive to 3-methyladenine and some amino acids. The present data indicate the lack of autophagosomal fusion with the inclusion because it was devoid of monodansylcadaverine and no distinct rim of autophagosomal protein-specific staining around the inclusion could be observed. However, high sensitivity of Chlamydia to conditions that could inhibit host autophagic pathway and the close association of MAP-LC3 and calreticulin with the inclusion membrane still suggest a potential role of host autophagy in the pathogenesis of Chlamydia.

* Corresponding author. Mailing address: Max Planck Institute for Infection Biology, Department of Molecular Biology, Schumannstr. 21/22, D-10117 Berlin, Germany. Phone: (49) 30-284-60-400. Fax: (49) 30-284-60-401. E-mail: meyer{at}mpiib-berlin.mpg.de.

Editor: J. N. Weiser

Infection and Immunity, August 2004, p. 4751-4762, Vol. 72, No. 8
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.8.4751-4762.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Braun, P. R., Al-Younes, H., Gussmann, J., Klein, J., Schneider, E., Meyer, T. F. (2008). Competitive Inhibition of Amino Acid Uptake Suppresses Chlamydial Growth: Involvement of the Chlamydial Amino Acid Transporter BrnQ. J. Bacteriol. 190: 1822-1830 [Abstract] [Full Text]  
  • Swanson, M. S. (2006). Autophagy: Eating for Good Health. J. Immunol. 177: 4945-4951 [Abstract] [Full Text]  
  • Al-Younes, H. M., Gussmann, J., Braun, P. R., Brinkmann, V., Meyer, T. F. (2006). Naturally occurring amino acids differentially influence the development of Chlamydia trachomatis and Chlamydia (Chlamydophila) pneumoniae.. J Med Microbiol 55: 879-886 [Abstract] [Full Text]  
  • Beatty, W. L. (2006). Trafficking from CD63-positive late endocytic multivesicular bodies is essential for intracellular development of Chlamydia trachomatis. J. Cell Sci. 119: 350-359 [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»