Publication Details
Abstract
Background: Toxoplasma gondii is an obligate intracellular protozoan that causes severe disease in humans and animals. Macrophage-mediated host responses are important to understand pathogenesis and protective immunity. Objectives: To determine the relative mRNA expression of Arg1, iNOS and CD86 in peripheral blood of T. gondii infected mice. Methodology: Fifty-two BALB/c mice were in the infected group and twenty BALB/c mice were in the uninfected control group. Tissue cysts were inoculated intraperitoneally to establish infection. Whole blood was collected at 40 days post-inoculation, total RNA extracted and cDNA synthesized. Transcript levels were quantified by RT-qPCR and normalized to a validated reference gene by the 2^-ΔΔCt^ method. Results: All three genes were significantly upregulated (~2-fold) by infection with large effect sizes (Hedges’ g = 0.81-1.01): Arg1 (3.058 ± 1.647 vs. 1.513 ± 1.147; 2.02-fold; p = 0.0031), iNOS (3.159 ± 1.967 vs. 1.685 ± 0.895; 1.87-fold; p = 0.0024), CD86 (3.792 ± 1.797 vs. 2.094 ± 1.009; 1.81-fold; p = 0.0008). The ratio of Arg1 to iNOS was not different between controls and infected mice (0.90 vs. 0.97), suggesting co-induction of competing L-arginine pathways in a balanced manner, rather than classical M1/M2 polarization. Two-way ANOVA revealed a significant effect of infection (all p ≤ 0.032) but no effect of sex (all p ≥ 0.37) or infection × sex interaction (all p ≥ 0.96). Conclusions T. gondii infection elicits a sex-independent co-regulated transcriptional signature in peripheral blood that integrates microbicidal, co-stimulatory and immunoregulatory myeloid pathways, and represents a promising minimally invasive biomarker panel for monitoring host immune status.