Intestinal inflammation dictates galectin-1-induced apoptosis of epithelial cells

MUGLIA CECILIA; PAPA GOBBI RODRIGO; SMALDINI PAOLA; ORSINI DELGADO MARIA LUCIA; ZANUZZI CAROLINA; SAMBUELLI ALICIA; ROCCA ANDRES; TOSCANO MARTA; RABINOVICH GABRIEL; DOCENA GUILLERMO H.

Mardel Plata

Congreso; LXII Reunión Anual de la Sociedad Argentina de Inmunología; 2014

SAi y SAIC

Intestinal epithelial cells (IEC) are key players in mucosal homeostasis. When the epithelial barrier is impaired inflammatory disorders may arise, such as in IBD and allergy. Based on our previous findings on the role of Gal-1 in IEC apoptosis, we studied the influence of pro-inflammatory cytokines on the pro-apoptotic effect of this β-galactoside binding protein. IEC were isolated form Balb/c mice and incubated with different pro-inflammatory cytokines (IL-1β, IFN-γ, TNF-α, IL-5 and IL-13). Gal-1 binding and apoptosis were evaluated by flow cytometry using biotinylated Gal-1, annexinV/propidium iodide and JC1. To investigate the in vivo effect of an inflammatory Th1 or Th2 environment we performed these assays in IEC isolated from a TNBS-induced colitis and a cholera toxin-driven allergy model. Finally, we assessed Gal-1 binding and Gal-1-induced apoptosis by TUNEL (confocal microscopy) in IEC of IBD patients. We found increased binding of Gal-1 to IEC incubated with IL-1β, TNF-α or IL-13 (35±4; 55±13 and 76±8 compared to 9±2 of controls, P