Treatment of acute experimental allergic encephalomyelitis in the lewis rat with the sex-hormone progesterone

In the present study we examined the effect of treatment with progesterone on experimental allergic encephalomyelitis (EAE), an animal model for the human neurological disease multiple sclerosis (MS). Acute EAE was induced in female Lewis rats by immunization with guinea pig spinal cord. From 4 days before induction until 21 days after induction the rats-were treated with progesterone suspended in vehicle or with vehicle alone. All rats developed histological signs and clinical symptoms, characteristic for EAE. Treatment with progesterone: resulted in partial protection against the histological signs, but did not suppress the clinical symptoms. The hormone treatment had no effect on the thymus or spleen. Therefore we suggest that treatment with progesterone protected against the histological signs of EAE through a peripheral immune mechanism

SUPPRESSION OF ACUTE EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS BY THE SYNTHETIC SEX-HORMONE 17-ALPHA-ETHINYLESTRADIOL - AN IMMUNOLOGICAL STUDY IN THE LEWIS RAT

Induction of experimental allergic encephalomyelitis (EAE) in female Lewis rats led to the well-known clinical symptoms and histological signs. Treatment with the synthetic estrogen 17-alpha-ethinylestradiol (EE) from day -4 before induction until day 21 after induction resulted in partial suppression of these signs and symptoms. Analysis of the peripheral blood leukocyte (sub)populations in these treated animals indicated some remarkable changes. However, these changes were also observed without EE treatment. EE treatment of EAE rats resulted in a significant decrease of the relative weights of both thymus and spleen, which changes however were not reflected in the peripheral blood. Apparently the effects of EE treatment on EAE in the present experiments indicate an action locally at the site of the EAE lesion and do not seem to be mediated by gross changes in the levels of peripheral blood leukocytes

The effect of gonadectomy on the clinical course of chronic experimental allergic encephalomyelitis

Experimental allergic encephalomyelitis (EAE) is an animal model for the human neurological disease multiple sclerosis (MS). Upon immunization with guinea pig spinal cord under a low dose of Cyclosporin A, male Lewis rats develop a severe chronic (relapsing) course of EAE (CR-EAE). By contrast, female Lewis rats develop a more mitigated course of EAE: only half of the female rats develop relapses. To Further analyze factors determining this sexual dimorphism in the course of EAE, in the present study male and female Lewis rats were gonadectomized before induction of CR-EAE. Now both male and female rats all developed a severe chronic course of EAE, showing extensive pathological changes in the CNS. In the female sham-gonadectomy (control) group only one third of the rats developed relapses. These female rats only showed mild pathological changes in the CNS. In the male sham-gonadectomy (control) group all rats developed relapses of EAE and showed extensive pathological changes in the CNS. From these data we conclude that the presence of the ovaries (partially) protects female rats against relapses of EAE and CNS injury. Presence or absence of the testes apparently makes no difference on the course of EAE. We propose that sex hormones produced in the ovaries protect female rats against relapses of EAE and underlying CNS injury