Abstract
Desmosomes are junctional protein complexes that confer strong adhesive capacity to adjacent host cells. In a recent study, we showed that enteropathogenic Escherichia coli (EPEC) disrupts desmosomes, weakens cell-cell adhesion and perturbs barrier function of intestinal epithelial (C2(BBe)) cells. Desmosomal damage was dependent on the EPEC effector protein EspH and its inhibitory effect on Rho GTPases. EspH-mediated Rho inactivation resulted in retraction of keratin intermediate filaments and degradation of desmosomal cadherins. Immunofluorescence studies of EPEC-infected C2(BBe) cells revealed keratin retraction towards the nucleus coincident with significant cytoplasmic redistribution of the desmosomal cadherin desmoglein-2 (DSG2). In this addendum, we expand on how EPEC-induced keratin retraction leads to loss of DSG2 anchoring at the junctions, and show that maturity of the epithelial cell monolayer impacts the fate of desmosomes during infection.