A melhora funcional e morfológica do músculo distrófico com o uso de um bloqueador do receptor da interleucina 6

Itália - os autores pesquisaram uma maneira de tratar a distrofia com anti-inflamatórios que tivessem menor quantidade de efeitos colaterais que os corticóides. A interleucina 6 está aumentada em pessoas e camundongos com distrofia muscular de Duchenne. Neste experimento em camundongos utilizaram um bloqueador do receptor da interleucina 6. Os animais tratados apresentaram melhora da força muscular e melhora das alterações patológicas demonstrando um efeito positivo e promissor para tratamento desta forma de distrofia muscular. 

O resumo em inglês pode ser lido abaixo:

(EBioMedicine, 2015) Functional and morphological improvement of dystrophic muscle by interleukin 6 receptor blockade

Laura Pelosi, Maria Grazia Berardinelli, Loredana De Pasquale, Carmine Nicoletti, Adele D’Amico, Francesco Carvello, Gian Marco Moneta, Angela Catizone, Enrico Bertini, Fabrizio De Benedetti, Antonio Musarò - Italy

The anti-inflammatory agents glucocorticoids (GC) are the only available treatment for Duchenne muscular dystrophy (DMD). However, long-term GC treatment causes muscle atrophy and wasting. Thus, targeting specific mediator of inflammatory response may be more specific, more efficacious, and with fewer side effects. The pro-inflammatory cytokine interleukin (IL) 6 is overproduced in patients with DMD and in the muscle of mdx, the animal model for human DMD. We tested the ability of inhibition of IL6 activity, using an interleukin-6 receptor (Il6r) neutralizing antibody, to ameliorate the dystrophic phenotype. Blockade of endogenous Il6r conferred on dystrophic muscles resistance to degeneration and alleviated both morphological and functional consequences of the primary genetic defect. Pharmacological inhibition of IL6 activity leaded to changes in the dystrophic muscle environment, favoring anti-inflammatory responses and improvement in muscle repair. This resulted in a functional homeostatic maintenance of dystrophic muscle.

These data provide an alternative pharmacological strategy for treatment of DMD and circumvents the major problems associated with conventional therapy.