This Article Full Text (PDF) 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 Reynolds, D J Articles by Pearce, J H Search for Related Content PubMed PubMed Citation Articles by Reynolds, D J Articles by Pearce, J H

 Previous Article  |  Next Article 

Infect Immun. 1991 September; 59(9): 3033-3039

Endocytic mechanisms utilized by chlamydiae and their influence on induction of productive infection.

D J Reynolds and J H Pearce

Microbial Molecular Genetics and Cell Biology Group, School of Biological Sciences, University of Birmingham, United Kingdom.

ABSTRACT

The microfilament-disrupting drug cytochalasin D and, initially, inoculation at 20 degrees C were used to differentiate between phagocytosis (sensitive to both treatments) and pinocytosis (resistant to both treatments) to assess whether chlamydial uptake into McCoy cells occurred by one or both mechanisms and whether each could contribute to productive infection. Both treatments suppressed the infectivity of Chlamydia trachomatis L2/434/Bu and C. psittaci GPIC (the guinea pig inclusion conjunctivitis strain) following static inoculation by only 50%, indicating that there was simultaneous operation of both phagocytosis and pinocytosis during uptake that led to productive infection. Measurement of the entry of organisms by two separate assays established that both strains predominantly used a cytochalasin D-resistant (pinocytic) mechanism, implying that phagocytic uptake was coupled to a higher frequency of productive infection. Integration of the data on infectivity and entry allowed the potential for an organism to infect a host cell to be quantified. This synthesis revealed that for both strains the infectivity potential following phagocytic entry was ca. 10-fold greater than that following pinocytic entry. However, both entry mechanisms were exploited more efficiently by strain L2/434/Bu than by strain GPIC (unless the latter was inoculated with centrifugation), indicating that intrinsic strain properties are more important for infectivity potential than the endocytic mechanism utilized.

---

Infect Immun. 1991 September; 59(9): 3033-3039

This article has been cited by other articles:

• Wuppermann, F. N., Molleken, K., Julien, M., Jantos, C. A., Hegemann, J. H. (2008). Chlamydia pneumoniae GroEL1 Protein Is Cell Surface Associated and Required for Infection of HEp-2 Cells. J. Bacteriol. 190: 3757-3767 [Abstract] [Full Text]  
• Hybiske, K., Stephens, R. S. (2007). Mechanisms of Chlamydia trachomatis Entry into Nonphagocytic Cells. Infect. Immun. 75: 3925-3934 [Abstract] [Full Text]  
• Carabeo, R. A., Grieshaber, S. S., Fischer, E., Hackstadt, T. (2002). Chlamydia trachomatis Induces Remodeling of the Actin Cytoskeleton during Attachment and Entry into HeLa Cells. Infect. Immun. 70: 3793-3803 [Abstract] [Full Text]  
• Raulston, J. E., Davis, C. H., Paul, T. R., Hobbs, J. D., Wyrick, P. B. (2002). Surface Accessibility of the 70-Kilodalton Chlamydia trachomatis Heat Shock Protein following Reduction of Outer Membrane Protein Disulfide Bonds. Infect. Immun. 70: 535-543 [Abstract] [Full Text]  
• BOLTON, A. J., OSBORNE, M. P., STEPHEN, J. (2000). Comparative study of the invasiveness of Salmonella serotypes Typhimurium, Choleraesuis and Dublin for Caco-2 cells, HEp-2 cells and rabbit ileal epithelia. J Med Microbiol 49: 503-511 [Abstract] [Full Text]