Aims Immunomodulatory effects of parasitic infections on the outcomes of allergic or autoimmune disorders have been addressed in many experimental studies. We examined the effects of Plasmodium yoelii 17X NL (Py) infection on collagen‐induced arthritis (CIA). Methods and Results Male DBA/1J mice were immunized with bovine type II collagen (IIC). Py inoculation was induced at three different time points (1, 4 weeks after or 4 weeks before the immunization). Only the inoculation at 4 weeks after IIC immunization significantly inhibited arthritis development. Non‐malarial anaemia induced by phenylhydrazine hydrochloride (PHZ) did not affect arthritis development. In the infected mice, anti‐IIC IgG levels were transiently reduced. In addition, splenic production of pro‐arthritic cytokines (IL‐17 and TNF‐α) and IFN‐γ decreased, whereas IL‐10 production increased. Flow cytometric analysis clarified that the main IL‐10 producers in Py‐infected mice had the CD4+CD25–Foxp3– phenotype, presumably Tr1 cells. Conclusion We demonstrated that experimental malarial infection alleviated autoimmune arthritis via immunomodulation, suggesting the importance of malaria in the hygiene hypothesis and the significance of searching for therapeutic immunomodulatory molecules from malarial parasites.

Background: Toxoplasmosis is a wide spread protozoan disease. It was generally believed that primary infection by T. gondii protects from reinfection, however, multiple cases of reinfection have been detected in immune mothers. This work reports results of re-infection of Swiss Webster (SW) mice with different strains of T. gondii. Objective: To simulate the impact of reinfection in experimentally infected mice with lethal strain of T. gondii after prime infection with non-virulent genotype. Material and Methods: The study was conducted on 36 female SW mice which were divided into four groups: 6 mice were infected with ME49 only (GI); 18 mice were infected with ME49 and re-challenged with RH on day 65, i.e. 8 weeks post ME49 infection (GII); 6 mice were infected with RH only (GIII); and 6 non-infected control mice (GIV). Toxoplasma RH strain re-challenged mice (GII) were monitored over two weeks observation period for mortality, clinical signs of acute illness (scored grades I-II), presence of intraperitoneal tachyzoites, brain cyst burden, and compared to chronically infected non-challenged mice (GI) and mice infected with RH only (GIII). Results: Prolonged survival rate of re-challenged group of mice than in RH only infected group was the only significant result. Cyst number and diameter were higher in re-challenged group than in mice infected only with ME49. Tachyzoites were recovered from peritoneal lavage of all mice that received RH whether primarily infected with ME49 or not. Clinical grading (I-II) was the same for both groups and both reached grade II. Conclusion: These results highlighted that mice with chronic toxoplasmosis developed acute disease when rechallenged with another virulent strain. Therefore, chronic infection with T. gondii apparently neither prevents acute disease nor impairs colonization of the brain with tissue cysts after virulent strain superinfection. The present work supports and explains the possibility of congenital toxoplasmosis in immune pregnant mothers when re-infected by a virulent strain of T. gondii.