Fig. 2. CNF-1 disrupts TJ gate function in a polarized intestinal epithelial monolayer. T84 monolayers were incubated basolaterally with increasing concentrations of CNF-1 (0.005-5 nM; n=4-12 monolayers) for 24 hours. CNF-1 evoked a concentration-dependent reduction in TER that was maximal at 1 nM (A). In parallel, monolayers were treated either apically (light gray, center) or basolaterally (dark gray) with 1 nM CNF-1 or with vehicle alone (black) for 24 hours (B). Permeation of apically loaded fluorosceinated dextran (FD-3; MW 3000) into the basal compartment over 2 hours was used as an index of passive paracellular transport. Flux of FD-3 across control monolayers and those treated apically with CNF-1 were virtually identical irrespective of CNF-1 incubation time. However, basolateral treatment with CNF-1 augmented FD-3 flux in a time-dependent fashion, which was statistically significant at t=24 and 48 hours (n10 monolayers per condition).

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