The epithelium is an active and key innate immunity component acting as a biological, chemical and physical barrier in mucosal tissues. Epithelial cell infection triggers its pyroptotic cell death and elimination from the monolayer to restore epithelia barrier function and homeostasis. However, the morphological features and molecular mechanisms associated with lytic death of an epithelial cell, and the resultant response of the monolayer, remains unknown. Herein we addressed this topic using genetic, pharmacological and live cell imaging techniques in colonic epithelial monolayers expressing an activatable Caspase1 (Casp1) system. Casp1 activation leads to Casp1 and GSDMD cleavage and sequential membrane permeabilization; features of pyroptotic (lytic) cell death. In epithelial monolayers, lytic cell death is followed by apical/luminal elimination of the dead cell, due to rearrangement of the neighbouring cells. Strikingly, and distinct from epithelial cell apoptosis, epithelial cell lytic death leads to breaks in cell-cell junctions and a transient increase in monolayer permeability. Also, lytic cell death triggers neighbouring cells to produce lamellipodia and membrane ruffles but rarely actin rings. Pharmacological inhibition of these structures considerably delayed resealing of the epithelial monolayer. To address forces generated by these structures, we used Traction Force Microscopy. Curiously, epithelial pyroptosis induces force signatures in neighbours that resemble a lamellipodia-driven mechanism for monolayer resealing; this involves outward forces generated by cell crawling and inward forces generated by actin cables. Collectively our results show that lytic cell death in epithelial tissues induces a transient break in barrier function and compared to apoptosis, a distinct mechanism for eliminating the dead cell from the monolayer.