Skip to main content
. 2003 Dec;71(12):7069–7078. doi: 10.1128/IAI.71.12.7069-7078.2003

FIG. 2.

FIG. 2.

Confocal micrographs show that EPEC infection allows β1-integrin to migrate to the apical membrane. (A) Uninfected monolayers and those infected with EPEC for 6 h were immunostained with antibodies to β1-integrin. Note that in uninfected monolayers the staining for β1-integrin is basolateral and limited to the lateral membrane. EPEC-infected monolayers revealed a significant presence of β1-integrin at the apical pole of the cells, indicating free access and redistribution to the apical membrane after infection. Data are presented as yz single focal planes. (B) Confocal microscopy of uninfected and EPEC-infected monolayers dual labeled for actin (red) and β1-integrin (green). In uninfected monolayers the β1-integrin is primarily limited to the basal surface, with some lateral localization, but restricted to the region basolateral to the apical actin-myosin ring. (C) Following EPEC infection, apically localized regions of actin aggregation are seen and correspond with microcolony attachment as viewed by differential interference contrast microscopy. Colocalization of β1-integrin to the same A/E lesions is indicated by a yellow signal.