Recombinant Mouse Prolactin Confers Partial Protection Against Toxoplasma gondii Infection in a Pre-treated Experimental Murine Model.

INTRODUCTION: Toxoplasmosis is one of the most important health-threatening diseases with worldwide distribution and global impact. It is caused by Toxoplasma gondii (T. gondii), an intracellular apicomplexan parasite that can evade the host immune responses and establish a chronic infection. The available treatments are not efficient against this stage and have many adverse effects. There are no available effective vaccines, apart from Toxovax®, which is used in sheep to prevent abortion. Studies documented that prolactin (PRL) had in vivo and in vitro anti-Toxoplasma effects. Detailed research was recommended about the mechanisms of such inhibitory effects. AIM: This study was designed to assess the possible protective role of the recombinant prolactin (rPRL) against T. gondii. MATERIALS AND METHODS: Sixty experimentally infected mice with T. gondii were used. The treated mice received rPRL for five days before infection. Serum prolactin levels were measured; survival rate was monitored; number, size, and DNA of T. gondii cysts in the brain were measured; and histopathological and immunological studies were done. RESULTS: There was a significant increase in the survival rate of the rPRL-treated mice, a significant decrease in the number, size, and DNA amount of T. gondii cysts in the brain with a noticeable improvement of histopathological lesions in the brain and liver tissues when compared to the infected untreated group. These effects seem to be achieved through stimulating humoral and cell-mediated immune responses that were evident by the significant rise in serum levels of anti-Toxoplasma IgM, IFN-γ, and TNF-α. CONCLUSION: The rPRL elicited robust immune responses, which provided efficient protection against murine T. gondii infection.

IL-10 polymorphisms and T-cell subsets could affect the clinical presentation and outcome of childhood immune thrombocytopenia in Egyptian population.

The aim is to study IL-10 polymorphisms and IL-10 level and assess their relation to T-cell subsets in childhood immune thrombocytopenia (ITP). In all, 40 (25 acute, 15 chronic) ITP child patients were investigated at time of presentation, compared to 15 healthy, age- and gender-matched controls and followed up for 1 year to determine chronic cases. Studying the effect of IL-10 promoter polymorphism was done by PCR-RFLP, IL-10 level was determined by ELISA, natural killer cells and T-cell subsets were evaluated by flow cytometry. Subjects with IL-10 promoter (1082 AA and 592 AA) genotypes had lower IL-10 levels and had lower CD4%, higher CD8%, lower CD4/CD8 ratio and lower T-reg%. IL-10 polymorphisms had no effect on NK%. IL-10 serum levels and IL-10 promoter polymorphic genotype frequencies are not different between ITP cases and controls; however, in ITP patients, IL-10 promoter (1082 AA and 592 AA) genotypes and associated lower CD4, higher CD8, lower CD4/CD8 ratio is associated with more severe thrombocytopenia at presentation and had a poorer response to first-line treatment. Patients with lower T-reg cells had a higher tendency to develop chronic ITP. IL-10 level and polymorphisms as well as disturbed T-cell subsets percentages are demonstrable effectors of immune dysfunction in ITP and can affect the presentation and outcome of childhood ITP.