Study summary · research use only
Induction of experimental autoimmune orchitis in mice: responses to elevated circulating levels of the activin-binding protein, follistatin
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study in mice examined experimental autoimmune orchitis (EAO), a rodent model of chronic testicular inflammation, in relation to elevated circulating follistatin, an activin antagonist. Before EAO induction, mice received an intramuscular injection of a viral vector carrying the circulating form of follistatin, FST315 (FST group), or an empty vector (EV group). Serum follistatin was increased 5-fold in the FST group versus the EV group at 30 and 50 days of EAO, though intra-testicular follistatin and activin A were not significantly changed. EAO induction was reduced but not prevented, with mild-to-severe damage in 75% of the EV group and 40% of the FST group at 50 days after immunisation. The authors state activin A is implicated in EAO progression and that elevated follistatin was not sufficient to prevent EAO development.
Abstract
Experimental autoimmune orchitis (EAO) is a rodent model of chronic testicular inflammation that mimics the pathology observed in some types of human infertility. In a previous study, testicular expression of the inflammatory/immunoregulatory cytokine, activin A, was elevated in adult mice during the onset of EAO, indicating a potential role in the regulation of the disease. Consequently, we examined the development of EAO in mice with elevated levels of follistatin, an endogenous activin antagonist, as a potential therapeutic approach to testicular inflammation. Prior to EAO induction, mice received a single intramuscular injection of a non-replicative recombinant adeno-associated viral vector carrying a gene cassette of the circulating form of follistatin, FST315 (FST group). Serum follistatin levels were increased 5-fold in the FST group compared with the control empty vector (EV) group at 30 and 50 days of EAO, but intra-testicular levels of follistatin or activin A were not significantly altered. Induction of EAO was reduced, but not prevented, with mild-to-severe damage in 75% of the EV group and 40% of the FST group, at 50 days following immunisation with testicular homogenate. However, the EAO damage score (based on disruption of the blood-testis barrier, apoptosis, testicular damage and fibrosis) and extent of intratesticular inflammation (expression of inflammatory mediators) were directly proportional to the levels of activin A measured in the testis at 50 days. These data implicate activin A in the progression of EAO, thereby providing a potential therapeutic target; however, elevating circulating follistatin levels were not sufficient to prevent EAO development.
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