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Modulation of Early β-Defensin-2 Production as a Mechanism Developed by Type I Toxoplasma gondii To Evade Human Intestinal Immunity
- Morampudi, Vijay, Braun, Michel Y., D'Souza, Sushila
- Infection and immunity 2011 v.79 no.5 pp. 2043-2050
- Toxoplasma gondii, gene activation, gene expression, genes, genotype, humans, immune evasion, innate immunity, intestinal mucosa, parasites, pathogenicity, transcriptomics, viability
- 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, β-defensins distinguished the most IEC infected by fast- or slow-replicating T. gondii genotypes. Although β-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 β-defensin 2 gene expression. Notably, no β-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 β-defensin 2 significantly reduced their infectivity of IEC. These findings strongly support the modulation of early β-defensin 2 expression as a mechanism used by type I T. gondii parasites to mediate immune evasion.