Dh. Meyer et al., MODELS OF INVASION OF ENTERIC AND PERIODONTAL PATHOGENS INTO EPITHELIAL-CELLS - A COMPARATIVE-ANALYSIS, Critical reviews in oral biology and medicine, 8(4), 1997, pp. 389-409
Bacterial invasion of epithelial cells is associated with the initiati
on of infection by many bacteria. To carry out this action, bacteria h
ave developed remarkable processes and mechanisms that co-opt host cel
l function and stimulate their own uptake and adaptation to the enviro
nment of the host cell. Two general types of invasion processes have b
een observed. In one type, the pathogens (e.g., Salmonella and Yersini
a spp.) remain in the vacuole in which they are internalized and repli
cate within the vacuole. In the other type, the organism (e.g., Actino
bacillus actinomycetemcomitans, Shigella flexneri, and Listeria monocy
togenes) is able to escape from the vacuole, replicate in the host cel
l cytoplasm, and spread to adjacent host cells. The much studied enter
opathogenic bacteria usurp primarily host cell microfilaments for entr
y. 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 invasiv
e periodontopathogens, A. actinomycetemcomitans and Porphyromonas (Bac
teroides) gingivalis, reveal that these bacteria have developed invasi
on strategies and mechanisms similar to those of the enteropathogens.
Entry of A. actinomycetemcomitans is mediated by microfilaments, where
as entry of P. gingivalis is mediated by both microfilaments and micro
tubules. A, actinomycetemcomitans, like Shigella and Listeria, can esc
ape 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 ca
use acute diseases, such as dysentery, have developed similar invasion
strategies.