Models of Invasion of Enteric and Periodontal Pathogens Into Epithelial Cells: A Comparative Analysis
- 1 October 1997
- journal article
- research article
- Published by SAGE Publications in Critical Reviews in Oral Biology & Medicine
- Vol. 8 (4), 389-409
- https://doi.org/10.1177/10454411970080040301
Abstract
Bacterial invasion of epithelial cells is associated with the initiation of infection by many bacteria. To carry out this action, bacteria have developed remarkable processes and mechanisms that co-opt host cell function and stimulate their own uptake and adaptation to the environment of the host cell. Two general types of invasion processes have been observed. In one type, the pathogens (e.g., Salmonella and Yersinia spp.) remain in the vacuole in which they are internalized and replicate within the vacuole. In the other type, the organism (e.g., Actinobacillus actinomycetemcomitans, Shigella flexneri, and Listeria monocytogenes) is able to escape from the vacuole, replicate in the host cell cytoplasm, and spread to adjacent host cells. The much-studied enteropathogenic bacteria usurp primarily host cell microfilaments for entry. Those organisms which can escape from the vacuole do so by means of hemolytic factors and C type phospholipases. The cell-to-cell spread of these organisms is mediated by microfilaments. The investigation of invasion by periodontopathogens is in its infancy in comparison with that of the enteric pathogens However, studies to date on two invasive periodontopathogens, A. actinomycetemcomitans and Porphyromonas (Bacteroides) gingivalis, reveal that these bacteria have developed invasion strategies and mechanisms similar to those of the enteropathogens. Entry of A. actinomycetemcomitans is mediated by microfilaments, whereas entry of P. gingivalis is mediated by both microfilaments and microtubules. A. actinomycetemcomitans, like Shigella and Listeria, can escape from the vacuole and spread to adjacent cells. However, the spread of A. actinomycetemcomitans is linked to host cell microtubules, not microfilaments. The paradigms presented establish that bacteria which cause chronic infections, such as periodontitis, and bacteria which cause acute diseases, such as dysentery, have developed similar invasion strategies.Keywords
This publication has 196 references indexed in Scilit:
- Requirement of CDC42 for Salmonella -Induced Cytoskeletal and Nuclear ResponsesScience, 1996
- The actin‐based motility of the facultative intracellular pathogen Listeria monocytogenesMolecular Microbiology, 1994
- Microtubule inhibitors differentially affect translational movement, cell surface expression, and endocytosis of transferrin receptors in K562 cellsJournal of Cellular Physiology, 1994
- Fc-binding components: a virulence factor in Actinobacillus actinomycetemcomitans?Oral Microbiology and Immunology, 1991
- Immunobiological activities of synthetic peptide segments of fimbrial protein from Porphyromonas gingivalisBiochemical and Biophysical Research Communications, 1991
- Signal transduction by receptors with tyrosine kinase activityCell, 1990
- Role of hemolysin for the intracellular growth of Listeria monocytogenes.The Journal of Experimental Medicine, 1988
- Integrins: A family of cell surface receptorsCell, 1987
- Collagenolytic activity associated with Bacteroides species and Actinobacillus actinomycetemcomitansJournal of Periodontal Research, 1982
- Comparative ultrastructure of leukotoxic and non‐leukotoxic strains of Actinobacillus actinomycetemcomitansJournal of Periodontal Research, 1981