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This is not surprising considering that the cellular receptors mediating spore entry into these two types of cells are almost certain to be distinct.
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However, prior to this study little information was available regarding the molecular mechanism of spore-epithelium interactions, what factors mediate spore entry into epithelial cells or the biological consequence of disrupting the entry process.
The results from the transwell assays indicate that inhibition of Src-mediated spore entry dramatically reduced B. anthracis dissemination through epithelial cells.
Therefore, we investigated the connection between PI3K and c-Src in mediating spore uptake by epithelial cells.
These results suggest that both the side chain length and presence of a charge at Ssp4 residue 36 may be important for mediating spore resistance properties.
Over expression of exogenous wide-type p85α did not increase spore internalization, possibly because the amount of endogenous adaptors was sufficient to mediate spore internalization (Fig. 2, E and Fig. S1, D).
We tested if spore entry into epithelial cells was mediated by a class IA PI3K.
These results indicated that specific components on B. anthracis spores were necessary and sufficient to induce spore entry into non-phagocytic cells.
In this study we sought to determine the molecular events involved in spore entry into lung epithelial cells.
SU6656 at a concentration of 50 µM significantly inhibited spore entry into A549 cells by approximately 70% (data not shown).
These results suggested that both PI3K and c-Src are involved in regulating actin polymerization during spore entry.
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