Evaluation of the PEIII-LC3-KDEL3 Chimeric Protein of Lectin as a Vaccine Candidate against Amebic Liver Abscess.

is an intestinal parasite that causes dysentery and amebic liver abscess. has the capability to invade host tissue by union of virulence factor Gal/GalNAc lectin; this molecule induces an adherence-inhibitory antibody response as well as to protect against amebic liver abscess (ALA). The present work showed the effect of the immunization with PEIII-LC3-KDEL3 recombinant protein. , this candidate vaccine inhibited adherence of trophozoites to HepG2 cell monolayer, avoiding the cytolysis, and in a hamster model, we observed a vaccine-induced protection against the damage to tissue liver and the inhibition of uncontrolled inflammation. PEIII-LC3-KDEL3 reduced the expression of TNF-, IL-1, and NF-B in all immunized groups at 4- and 7-day postinfection. The levels of IL-10, FOXP3, and IFN- were elevated at 7 days. The immunohistochemistry assay confirmed this result, revealing an elevated quantity of +IFN- cells in the liver tissue. ALA formation in hamsters immunized was minimal, and few trophozoites were identified. Hence, immunization with PEIII-LC3-KDEL3 herein prevented invasive amebiasis, avoided an acute proinflammatory response, and activated a protective response within a short time. Finally, this recombinant protein induced an increase of serum IgG.