Models of invasion of enteric and periodontal pathogens into epithelial cells: a comparative analysis.
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.
Meyer
D H
DH
Department of Microbiology and Molecular Genetics, University of Vermont, Burlington 05405, USA.
Mintz
K P
KP
Fives-Taylor
P M
PM
D008841:Actin Cytoskeleton / Q000382:microbiology; D016976:Aggregatibacter actinomycetemcomitans / Q000254:growth & development / Q000502:physiology*; D002455:Cell Division; D002908:Chronic Disease; D003593:Cytoplasm / Q000382:microbiology; D004755:Enterobacteriaceae / Q000254:growth & development / Q000502:physiology*; D004847:Epithelial Cells / Q000382:microbiology* / Q000648:ultrastructure; D006460:Hemolysin Proteins / Q000502:physiology; D006801:Humans; D008089:Listeria monocytogenes / Q000502:physiology; D008870:Microtubules / Q000382:microbiology; D010518:Periodontitis / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000254:growth & development / Q000502:physiology*; D012475:Salmonella / Q000502:physiology; D012763:Shigella flexneri / Q000502:physiology; D010738:Type C Phospholipases / Q000502:physiology; D014617:Vacuoles / Q000382:microbiology; D015007:Yersinia / Q000502:physiology
D006460:Hemolysin Proteins; D010738:Type C Phospholipases