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Objective:Inflammation plays an essential role in epilepsy. Studies indicate that cytokines and neurotrophic factors can act in neuroexcitability and epileptogenesis. We aimed to investigate the association between plasma inflammatory and neurotrophic markers, seizure frequency, and chronic epilepsy subtypes.Methods:We studied 446 patients with epilepsy and 166 healthy controls. We classified patients according to etiology and seizure frequency. We measured plasma levels of interleukin-1 (IL-1), IL-2, IL-4, IL-6, IL-10, IL-17, interferon-γ (IFNγ), tumor necrosis factor α (TNFα), soluble TNF receptor 1 (sTNFr1), sTNFr2, brain-derived neurotrophic factor (BDNF), neurotrophic factor 3 (NT3), NT4/5, ciliary neurotrophic factor (CNTF), nerve growth factor (NGF), and glial cell line-derived neurotrophic factor (GDNF) by enzyme-linked immunosorbent assay or cytometric bead array. Results:The plasma levels of BDNF, NT3, NGF, and sTNFr2 were higher, whereas IL-2, IL-4, IL-6, IL-10, IL-17, IFNγ, TNFα, CNTF, and sTNFr1 were lower in patients than controls. IL1, GDNF, and NT4/5 were similar between groups. These markers did not correlate with age, sex, and epilepsy duration.The molecule sTNFr2 was the best marker to discriminate patients from controls (area under the curve = .857), also differing between patients with frequent and infrequent seizures.Significance:This large cohort confirmed that patients with epilepsy have abnormal levels of plasma inflammatory and neurotrophic markers independent of the underlying etiology. Plasma level of sTNFr2 was related to seizure frequency and discriminated people with or without epilepsy with good accuracy, making it a potential biomarker for epilepsy and seizure burden.

Chagas disease is a parasitic infection with high socioeconomic impact throughout Latin America. Although this severe, incurable disease can be transmitted by several routes, oral transmission is currently the most important route in the Amazon Basin. Açaí pulp has nutritional properties and is popular throughout Brazil and abroad. However, this pulp has been associated with microepidemics of acute Chagas disease (ACD) in northern Brazil, where açaí fruit is the main food supplement. In this study, we examined the in vitro survival and in vivo virulence of Trypanosoma cruzi Y strain in açaí pulp. Aliquots of in natura açaí pulp produced in Belém city in the northern Brazilian state of Pará were mixed with 10⁵ trypomastigotes. The samples were incubated at room temperature or at 4 or -20°C for various periods, and the parasites were isolated by forced sieving. The resulting eluates were examined by microscopy, and the trypomastigotes were administered intraperitoneally, orally, or by gavage to immunodeficient mice (C.B-17-Prkdc(scid)/PasUnib) that had been pretreated with antibiotics. Parasitemia was quantified by the Brener method, and mortality was recorded daily. All routes of administration resulted in ACD. A 5-day delay in the onset of parasitemia occurred with oral administration. The survival and virulence of the parasites were unaffected by prior incubation at room temperature for 24 h, at 4°C for 144 h, and at -20°C for 26 h. These results indicate that T. cruzi can survive and retain its virulence in açaí pulp under various conditions and that cooling and freezing are not suitable methods for preventing foodborne ACD.

Outbreaks of acute Chagas disease (ACD) in northern Brazil can be caused by the ingestion of unprocessed açai pulp contaminated with Trypanosoma cruzi . The aim of this study was to determine the minimum thermal process required to inactivate T. cruzi in açai pulp. Trypomastigotes (100,000) of T. cruzi Y strain were added to 0.15 M NaCl or açai pulp and continuously mixed while being heat treated at 37 to 49°C for up to 1 h. When necessary, parasites were separated from açai pulp by forced sieving. Inocula were administrated intraperitoneally in inbred immunodeficient C.B-17-Prkdc/Pas Unib mice, and the recipients were monitored for parasitemia and mortality. Mice received prophylactic antibiotic therapy by using cephalexin to prevent bacterial infection from the açai pulp. T. cruzi retained its virulence in 0.15 M NaCl and açai pulp at 44 ± 0.1°C for 10 min and at 43 ± 0.1°C for 20 min, respectively, causing ACD and death in mice up to 24 days after infection. Incubation of açai pulp inoculum above 43°C for 20 min neutralized T. cruzi virulence, thereby preventing ACD and death in murine recipients. The heating of açai pulp above 43°C for 20 min is a practical and effective measure to prevent foodborne ACD caused by T. cruzi .