Toxoplasma gondii is known to cause congenital infection in humans and animals and severe disease in immunocompromised individuals; consequently development of vaccines against the parasite is highly necessary. Under stress conditions, T. gondii expresses the highly immunogenic heat shock protein 70 (TgHSP70). Here, we assessed the protective efficacy of rTgHSP70 immunization combined with Alum in oral ME-49 T. gondii infection and the mechanisms involved on it. It was observed that immunized mice with rTgHSP70 or rTgHSP70 adsorbed in Alum presented a significantly reduced number of cysts in the brain that was associated with increased iNOS+ cell numbers in the organ, irrespective the use of the adjuvant. Indeed, ex vivo experiments showed that peritoneal macrophages pre-stimulated with rTgHSP70 presented increased NO production and enhanced parasite killing, and the protein was able to directly stimulate B cells towards antibody producing profile. In addition, rTgHSP70 immunization leads to high specific antibody titters systemically and a mixed IgG1/IgG2a response, with predominance of IgG1 production. Nonetheless, it was observed that the pretreatment of the parasite with rTgHSP70 immune sera was not able to control T. gondii internalization and replication by NIH fibroblast neither peritoneal murine macrophages, nor anti-rTgHSP70 antibodies were able to kill T. gondii by complement-mediated lysis, suggesting that these mechanisms are not crucial to resistance. Interestingly, when in combination with Alum, rTgHSP70 immunization was able to reduce inflammation in the brain of infected mice and in parallel anti-rTgHSP70 immune complexes in the serum. In conclusion, immunization with rTgHSP70 induces massive amounts of iNOS expression and reduced brain parasitism, suggesting that iNOS expression and consequently NO production in the brain is a protective mechanism induced by TgHSP70 immunization, therefore rTgHSP70 can be a good candidate for vaccine development against toxoplasmosis.

Introduction: Vertically transmitted infections are caused by a diversity of pathogenic microorganisms. Pregnant women are routinely screened to evaluate the risks and reduce the burden of disorders in their unborn children. We assessed the prevalence and possible risk factors for Cytomegalovirus (CMV), Rubella, Human T lymphotropic virus (HTLV), and Toxoplasma gondii in pregnant women from the South region of Bahia State, Brazil. Methodology: Serum samples were obtained from 726 pregnant women aged between 13 and 44 years, with a median age of 24 years. ELISA assays were used to detect CMV, Rubella, HTLV and T. gondii IgG and IgM antibodies. Results: The prevalence rates of IgG antibodies found were 95.2% for CMV, 97.0% for Rubella, and 72.3% for T. gondii. Furthermore, the prevalence of HTLV-1/2 was 1.2%. IgM antibodies were reactive only for CMV (0.8%) and T. gondii (3.7%). Variables independently associated with the detection of anti-T. gondii IgG antibodies were white self-reported race/ethnicity (Odds Ratio [OR] 2.26, 95% CI 1.26–4.06, P = 0.006), wage income (OR 0.55, 95% CI 0.35–0.88, P = 0.013), and history of previous pregnancy (OR 1.60, 95% CI 1.02–2.50, P = 0.038). Conclusions: This study highlights the importance of monitoring for infectious diseases during pregnancy and initiation of early interventions to reduce the burden of fetal losses and other important infant sequelae attributable to congenital infections.

Iron is an important constituent of our environment, being necessary for both mammalian and pathogenic protozoa survival. Iron-containing proteins exert a wide range of biological processes such as biodegradation and biosynthesis, as well as immune function, fetal development, and physical and mental well-being. This work aimed to investigate the effect of iron deprivation in Toxoplasma gondii infection outcome. C57BL/6 mice were orally infected with T. gondii and treated with an iron chelator, deferoxamine, or supplemented with iron (ferrous sulfate), and the parasitism as well as immunological and histological parameters were analyzed. It was observed that the infection increased iron accumulation in the organs, as well as systemically, and deferoxamine treatment diminished the iron content in serum samples and intestine. The deferoxamine treatment decreased the parasitism and inflammatory alterations in the small intestine and lung. Additionally, they partially preserved the Paneth cells and decreased the intestinal dysbiosis. The ferrous sulfate supplementation, despite not significantly increasing the parasite load in the organs, increased the inflammatory alterations in the liver. Together, our results suggest that iron chelation, which is commonly used to treat iron overload, could be a promising medicine to control T. gondii proliferation, mainly in the small intestine, and consequently inflammation caused by infection.

The heat shock protein of Toxoplasma gondii (TgHSP70) is a parasite virulence factor that is expressed during T. gondii stage conversion. To verify the effect of dexamethasone (DXM)-induced infection reactivation in the TgHSP70-specific humoral immune response and the presence of the protein in the mouse brain, we produced recombinant TgHSP70 and anti-TgHSP70 IgY antibodies to detect the protein, the specific antibody and levels of immune complexes (ICs) systemically, as well as the protein in the brain of resistant (BALB/c) and susceptible (C57BL/6) mice. It was observed higher TgHSP70-specific antibody titers in serum samples of BALB/c compared with C57BL/6 mice. However, the susceptible mice presented the highest levels of TgHSP70 systemically and no detection of specific ICs. The DXM treatment induced increased parasitism and lower inflammatory changes in the brain of C57BL/6, but did not interfere with the cerebral parasitism in BALB/c mice. Additionally, DXM treatment decreased the serological TgHSP70 concentration in both mouse lineages. C57BL/6 mice presented high expression of TgHSP70 in the brain with the progression of infection and under DXM treatment. Taken together, these data indicate that the TgHSP70 release into the bloodstream depends on the death of the parasites mediated by the host immune response, whereas the increased TgHSP70 expression in the brain depends on the multiplication rate of the parasite.

Diabetic neuropathy (DN) is one of the main complications of diabetes mellitus (DM), responsible for a high morbimortality rate and burdening public health resources. Photobiomodulation has proven to be effective in relieving pain, reducing the inflammation, and improving vascularization. We report an evaluation of the effectiveness of photobiomodulation for the relief of pain and to improve the quality of life in patients with diabetic neuropathy. A total of 30 diabetic volunteers with DN were randomly divided into three groups: control, photobiomodulation (PBM), and placebo (P-PBM). Those in Group control were instructed to take diabetic neuropathy medication for 30 days. The PBM group received laser photobiomodulation treatment with the following protocol: three sessions per week for 30 days, totaling 12 applications (wavelength, 808 nm; energy density, 12 J/cm²). in the of following nerves: tibial medial plantar, own plantar digital, common plantar digital, superficial fibular, deep fibular, sciatic, saphenous, and common fibular. Patients in the P-PBM Group were submitted to the PBM protocol, but with the device switched off. Before and after applying the therapeutic protocols, all volunteers were subjected to pain evaluations. The results showed a statistically significant difference between the groups (p < 0.05). The PBM group confirmed an analgesic effect directly related to the use of the photobiomodulation, whilst the patients in group control and P-PBM, did not present significant results. The study demonstrated that laser photobiomodulation is effective in significantly reducing pain and improving the quality of life of patients with diabetic neuropathy.