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Background: During pregnancy, the balanced dominance of the T helper17 response shifts to a Th2 response that is characterised by the production of IL-10, following the completion of the implantation process. Transforming growth factor-β (TGF-β) expression is associated with the completion of trophoblast invasion and placental growth. This study assessed the effect of malaria infection on the levels of IL-17, IL-10, and TGF-β in the plasma of pregnant mice with malaria. Methods: Seventeen pregnant BALB/C mice were divided into two groups: mice infected with Plasmodium berghei (treatment group) and uninfected mice (control group). The mice were sacrificed on day 18 post-mating. Parasitemia was measured by Giemsa staining. The levels of IL-17, IL-10, and TGF-β were measured by ELISA. Results: Using independent t test, the IL-17 levels in the treatment group were higher than those in the control group (P = 0.040). The IL-10 levels in the treatment group were lower than those in the control group (P = 0.00). There was no significant difference in the TGF-β levels (P = 0.055) between two groups. However, using SEM analysis the degree of parasitemia decreased the plasma TGF-β levels (tcount = 5.148; ≥ ttable= 1.96). SEM analysis showed that a high degree of parasitemia increased the IL-17 levels and decreased the IL-10 and TGF-β levels. Conclusion: Malaria infection during pregnancy interferes with the systemic balance by increasing the IL-17 levels and decreasing the IL-10 and TGF-β levels. [ABSTRACT FROM AUTHOR]

Background: The innate immune response to tuberculosis infection may involve the increased production of nitric oxide and cathelicidin due to the up-regulated expression of the vitamin D receptor (VDR), though this proposed mechanism remains controversial. The aim of this study was to determine how the exposure of human monocytes to Mycobacterium tuberculosis (M. tuberculosis) DNA affects the production of nitric oxide and cathelicidin, as well as the expression of VDR. Methods: This study was performed using monocytes obtained from healthy donors. After 24 h incubation, monocytes were stimulated with M. tuberculosis DNA for 18 h to determine the expression of VDR mRNA and the production of nitric oxide and cathelicidin versus non-stimulated cells (the control group). Results: The expression of VDR mRNA was higher in the monocytes exposed to M. tuberculosis DNA compared to the control group (P = 0.020). Monocytes exposed to M. tuberculosis DNA also showed significantly increased production of nitric oxide and cathelicidin compared to the control group (P = 0.0001; P = 0.028). Conclusion: The stimulation of human monocytes with M. tuberculosis DNA increases the expression of the VDR mRNA and the production of nitric oxide and cathelicidin. [ABSTRACT FROM AUTHOR]