No abstract

Background: Therapeutic exercise has an important role to manage chemotherapy-induced peripheral neuropathy symptoms. However, there is little evidence of its effectiveness. Objective: To synthesize the evidence regarding therapeutic exercise during chemotherapy to improve peripheral neuropathy symptoms. Databases: PubMed, CINAHL, Cochrane Library, PEDro, ScienceDirect, Scopus, Web of Science and BIREME. Methodology: Randomized clinical trials were included. GRADE was used to synthesize evidence and an inverse variance model for meta-analysis. Results: Up to May 2022, 2172 references were analyzed and 14 studies that evaluated 1094 participants were included. The exercises were highly effective in improving pain threshold and moderately effective in improving peripheral neuropathy symptoms at the 8-week follow-up and the 4–24 weeks. Furthermore, the evidence was low in improving thermal threshold, tactile and vibratory sensitivity. Conclusion: Therapeutic exercise generates a significant reduction in peripheral neuropathy symptoms in patients in short- and long-term follow-up with a moderate level of evidence quality.

Trypanosomacruzi es el agente causal de la enfermedad de Chagas, la infección parasitaria más importante de Latinoamérica. Se considera una enfermedad crónica, que causa discapacidad, para la cual no existe tratamiento efectivo. Para poder establecer una infección de manera exitosa, T. cruzi cuenta con múltiples mecanismos para evadir la respuesta inmune del hospedero. Entre estos múltiples mecanismos, los tripomastigotes, formas infectantes del parásito, cuentan con mecanismos que los hacen resistir el ataque del sistema del complemento. Por el contrario, los epimastigotes son altamente susceptibles. Para resistir la lisis mediada por el complemento, T. cruziutilizadiversos factores que interfieren con las funciones de la ruta clásica o alterna en distintos puntos de la cascada. Sin embargo, estos mecanismos no son del todo comprendidos. Entre las proteínas que participan en la resistencia a la lisis están el factor acelerador del decaimiento de las convertasas de T. cruzi(T-DAF), la proteína reguladora del complemento de T. cruzi (CRP), calreticulina de T. cruzi(TcCRT), factor H, entre otras. A continuación revisaremos el rol de estas proteínas en la evasión del sistema del complemento del hospedero por T. cruzi.

Trypanosoma cruzi (T. cruzi), the causal agent of devastating Chagas disease, possesses multifactorial resistance to the alternative pathway (AP) of complement. AP regulatory protein factor H (fH) uses its C-terminal 19-20 domains to recognize polyanions (i.e. sialic acid) and C3b on host cells, facilitating decay of C3 convertases and inactivation of C3b via the N-terminus of fH. We have shown that recombinant C-terminal fH domains 19-20 (rH19-20) compete with fH for binding to C3b and host cell polyanions, inhibiting protection from the AP. T. cruzi tripomastigotes resist the AP by capturing sialic acid from host cells. The specific role that fH plays in protecting T. cruzi from the AP and the fH domains involved remain unknown. Here we assessed the susceptibility of T. cruzi (MF, Y and Brenner strains) to AP-mediated killing, and the ability of fH to bind directly to the parasite by FACS. For determining the fH domains needed for the interaction with T. cruzi, trypomastigotes were incubated with normal human sera in the presence or absence of equimolar amounts of overlapping recombinant fH proteins (2 to 3 domains each) spanning domains 7 to 20. The ability of each protein to increase AP-mediated killing of T. cruzi was assessed. Only rH19-20 effectively competed with serum fH, inducing a significant decrease in parasite survival (p<0.0001), indicating that the C-terminus of fH is essential for fH-mediated recognition and protection of T. cruzi trypomastigotes from the AP.