Barrier disruption in giardiasis and post-infection consequences. (1) Consumption of arginine via high arginine deaminase activity. Arginine starvation leads to an impaired secretion of anti-giardial Nitric Oxide (NO); (2) Giardia’s proteolytic activity (cathepsin-B-like cysteine proteases) lead to (3) An impairment of commensal microbiota biofilms, (4) the cleavage of pro-inflamatory chemokines (CXCL-8), (5) The disruption of MUC2 mucin integrity; (6) Diffuse shortening of brush border microvilli; (7) Disruption and/or rearrangement of the apical junction complex (AJC) (ZO-1, ZO-2, claudin-1, claudin-4, occludin), filamentous actin (F-actin and α-actinin), and at desmosomal level (desmocollin); (8) Bacterial and antigen translocation in the lamina propria; (9) Induction of pro-apoptotic factors caspase-3, 8 and 9, BAX, PARP, and impairment of anti-apoptotic protein Bcl-2; (10) Immune response in giardiasis is reviewed in Einarsson et al. 2016; (11) Toxic effects of pathobionts released by dysbiotic microbiota; (12) Paracellular translocation (13) Activation of pathogenic endocrine and immunological signals.2