Infection with avirulent type III secretion system-deficient strains of P. aeruginosa elicits the release of heat-stable amyloid antimicrobial peptides from microvascular endothelium, whereas endothelial intoxication with type III secretion system effectors, particularly ExoU and ExoY, potentiates the release of endothelium-derived dysregulated tau oligomers that appear to facilitate the conversion of endothelial amyloid antimicrobials into a virulent, self-propagating amyloid-tau species (34). This evidence concerns the gene MAPT and infection.