[Pidotimod inhibits activation of latent Toxoplasma gondii infection induced by dexamethasone in mice].

OBJECTIVE: To study the inhibition effect of pidotimod (PT) on dexamethasone (Dem)-induced reactivated toxoplasmosis in mice. METHODS: A total of 96 female BALB/C mice were infected orally with 30 cysts of Toxoplasma gondii TgCtwh6 strain (genotype Chinese 1). 4 weeks later the mice were divided into three groups (A, B, and C). Mice of group A (Dem+NS) were given Dem [6 mg/(kg x d)] intraperitoneally and 200 microl normal saline given orally. Mice of group B (Dem+PT) were orally given pidotimod [100 mg/(kg x d)] and intraperitoneally injected with Dem[6 mg/(kg x d)] simultaneously. Each mouse in group C received 200 microl normal saline intraperitoneally. The mice were injected and given by gavage for 5 weeks. After treatment, three mice in each group were scarified weekly, and the survival time of the mice was recorded in days. Brain parasite burden and T. gondii DNA copies in serum were detected by quantitative real-time PCR. T cell subsets, cytokine profiles in each group were analyzed by flow cytometry, and CBA kit, respectively. RESULTS: On the second week after Dem administration, parasitemia appeared in group A; in 5 weeks 50% mice had parasitemia again, and 17 mice died. Comparatively, in group B parasitemia appeared on the third week after PT and Dem administration, in 5 weeks 25% mice had parasitemia again, and 7 mice died. Parasitemia did not appear in Group C. On the 21st day after Dem administration, T. gondii DNA copies in brain tissues of group A was (209 +/- 12) x 10(9), significantly higher than (62 +/- 10) x 10(9) in group B treated with PT (n = 3, P < 0.01). Flow cytometry test showed that on the 21st day after Dem administration, the proportions of Th1, Th2 and Treg cells in groups A and B were (4.0 +/- .5)% and (6.1 +/- 1.0)%, (0.6 +/- 0.1)% and (0.5 +/- 0.2)%, and (5.0 +/- 0.9)% and (7.0 +/- 1.2)%, respectively. There was significant difference in the percentages of Th1 and Treg between group B and A (P < 0.01). The levels of IFN-gamma, TNF-alpha in group A were (2.2 +/- 0.7) pg/ml and (20.1 +/- 5.0) pg/ml, respectively, lower than that of group B [(3.6 +/- 0.6) pg/ml and (32.0 +/- 8.0) pg/ml] (P < 0.01). No statistical significance was found in the levels of IL-4 and IL-10 between group A [(2.6 +/- 0.4) pg/ml, (39.0 +/- 6.0) pg/ml] and group B [(2.7 +/- 0.7) pg/ml, (40.0 +/- 8.0) pg/ml] (P > 0.05). CONCLUSION: Pidotimod can inhibit activation of latent Toxoplasma gondii infection induced by dexamethasone in mice. Th1 and Treg cells may contribute to the pidotimod/dexamethasone-induced immunoregulation.

Infectivity of cysts of the ME-49 Toxoplasma gondii strain in bovine milk and homemade cheese

Objetivo: Analisar a infecciosidade e a resistência de cistos de T. gondii em leite e queijo fresco caseiro, pela infecção artificial de leite bovino. Métodos: O leite bovino pasteurizado foi infectado artificialmente com 10 cistos/ml de T.gondii cepa ME49 e inoculado em grupos de camundongos, imediatamente ou após ser estocado por 5, 10 e 20 dias a 4oC. Preparou-se queijo fresco caseiro com leite infectado, sendo testado em grupos de camundongos, utilizando a mesma conservação. A infecção foi detectada pela presença de cistos no cérebro dos camundongos desafiados ou testes sorológicos após cinco semanas, também confirmada por Western Blotting e histologia. Resultados: A infecciosidade dos cistos da cepa ME49 de T.gondii foi mantida mesmo quando armazenado no leite até 20 dias de conservação em condições de refrigeração a 4oC. Os cistos resistiram ao processo de fabricação do queijo e eram infectantes após um período de 10 dias nas mesmas condições. Conclusões: Os achados mostraram que o leite e seus derivados podem ser uma importante fonte de contaminação humana pelo T.gondii, reforçando a importância da pasteurização do leite antes de qualquer processamento ou ingestão