Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The calcium and phospholipid-binding proteins lipocortins 1, 2 and 5 have been detected, by electrotransfer and immunoblotting techniques, in central nervous system (CNS) tissues of control Lewis rats and animals with experimental allergic encephalomyelitis (EAE). The cerebellum and spinal cord content of lipocortins 2 and 5 remained unchanged throughout the development of EAE but the amounts of the steroid-inducible protein lipocortin 1 increased in samples from pre-diseased and adjuvant-treated rats and were further enhanced in tissues from clinically sick and convalescent animals. The significance of these findings is discussed in conjunction with the ongoing changes in pathology which occur during the progression of EAE.
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PMID:The detection of lipocortins 1, 2 and 5 in central nervous system tissues from Lewis rats with acute experimental allergic encephalomyelitis. 214 19

Spontaneous recovery from acute experimental allergic encephalomyelitis (EAE) by the Lewis rat is probably mediated by endogenous corticosteroids. It has been proposed that the anti-inflammatory actions of the glucocorticoids may be effected via the induction of mediator proteins termed lipocortins and recently we have demonstrated increased levels of lipocortin 1 in the central nervous system (CNS) of EAE-diseased rats (Bolton C., A-J. Elderfield and R.J. Flower (1990), J. Neuroimmunol. 29: 173-181). In this study, utilizing antisera raised against recombinant human lipocortin 1, immunohistochemistry and light microscopy have been used to determine the distribution of the protein in the cervical spinal cord of Lewis rats during EAE. In normal animals lipocortin 1 immunoreactivity was localized predominantly in the walls of larger blood vessels and to a lesser extent capillaries. The same staining pattern was found in adjuvant-inoculated controls. In sections from EAE-inoculated animals there was no change during the induction phase, but with the onset of clinical symptoms and the appearance of inflammatory infiltrates in the CNS, a marked increase in lipocortin 1 immunostaining was observed. This additional staining was due to widespread immunoreactivity of the lesions, was maximal at the height of disease and decreased following recovery and lesion regression. Within the lesions the vast majority of infiltrating lymphocytes and macrophages were positive for lipocortin 1, including some very heavily stained macrophage-like cells. Measurement of corticosterone in the sera of these animals showed that changes in lipocortin 1 immunostaining in the CNS during EAE closely parallel serum corticosterone levels.
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PMID:Lipocortin 1 (annexin 1) immunoreactivity in the cervical spinal cord of Lewis rats with acute experimental allergic encephalomyelitis. 827 28