Modulation of Early β-Defensin-2 Production as a Mechanism Developed by Type I Toxoplasma gondii To Evade Human Intestinal Immunity

We investigated the early innate immune responses induced in human intestinal epithelial cells (IEC) by the three defined Toxoplasma gondii genotype strains. Transcriptome analysis revealed that among differentially expressed genes, beta-defensins distinguished the most IEC infected by fast-or slow-replicating T. gondii genotypes. Although beta-defensin 1 and 3 genes were not expressed in host cells at early time points postinfection, the slow-replicating type II and III parasites induced high levels of beta-defensin 2 gene expression. Notably, no beta-defensin 2 gene expression occurred early after infection with the fast-replicating type I parasite. However, activation of this gene in IEC by poly(I:C) treatment prior to infection substantially decreased parasite viability, and pretreatment of parasites with synthetic beta-defensin 2 significantly reduced their infectivity of IEC. These findings strongly support the modulation of early beta-defensin 2 expression as a mechanism used by type I T. gondii parasites to mediate immune evasion.