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)

Prostaglandin (PG) and thromboxane levels were measured in the spinal cords and cerebellums of rats during the induction, disease and recovery periods of experimental allergic encephalomyelitis (EAE). In spinal cords PGE and 6-oxo-PGF1 alpha increased to maximum with the onset of neurological symptoms, 11-12 days after inoculation. However, the levels returned to normal at the height of clinical disease, despite the persistence of inflammatory lesions. After an initial fall, PGF2 alpha increased to normal limits, 11-12 days after inoculation, and remained at this level throughout the experiment. In contrast, the cerebellum content of all the eicosanoids decreased prior to the appearance of clinical EAE. PGF2 alpha and 6-oxo-PGF1 alpha concentrations subsequently increased but the PGE and thromboxane levels remained depressed for the duration of the study. The role of the eicosanoids in modulating the immune response to neuroantigen is discussed together with our recent findings in guinea pigs with acute EAE.
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PMID:Prostaglandin and thromboxane levels in central nervous system tissues from rats during the induction and development of experimental allergic encephalomyelitis (EAE). 660 9

Analysis of mRNA from multiple sclerosis lesions revealed increased amounts of transcripts for several genes encoding molecules traditionally associated with allergic responses, including prostaglandin D synthase, histamine receptor type 1 (H1R), platelet activating factor receptor, Ig Fc epsilon receptor 1 (Fc epsilon RI), and tryptase. We now demonstrate that, in the animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), mediated by T helper 1 (Th1) T cells, histamine receptor 1 and 2 (H1R and H2R) are present on inflammatory cells in brain lesions. Th1 cells reactive to myelin proteolipid protein expressed more H1R and less H2R than Th2 cells. Pyrilamine, an H1R antagonist, blocked EAE, and the platelet activating factor receptor antagonist CV6209 reduced the severity of EAE. EAE severity was also decreased in mice with disruption of the genes encoding Ig Fc gamma RIII or both Fc gamma RIII and Fc epsilon RI. Prostaglandin D synthase and tryptase transcripts were elevated in EAE brain. Taken together, these data reveal extensive involvement of elements of the immune response associated with allergy in autoimmune demyelination. The pathogenesis of demyelination must now be viewed as encompassing elements of both Th1 responses and "allergic" responses.
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PMID:Multiple elements of the allergic arm of the immune response modulate autoimmune demyelination. 1257 52

Diseases caused by immune inflammation, such as rheumatoid arthritis, multiple sclerosis, and Crohn's disease, are intractable diseases to which novel therapeutics are highly demanded. Prostaglandin (PG) E(2) is the most ubiquitously produced PG with various actions. PGE(2) has been traditionally regarded as an immunosuppressant based on its inhibition of T cell activation in vitro. However, in vivo relevance of the immunosuppressant action of PGE(2) has remained obscure. Recently, several groups including ourselves have made unexpected findings that PGE(2) facilitates expansion of the Th17 subset of T helper cells of both human and mouse through elevation of cAMP via PGE receptors EP2 and EP4. We have further found that PGE(2) can induce and not suppress Th1 differentiation under certain conditions, again, through EP2 and EP4. Given the putative roles of these Th subsets in immune diseases such as the above, these findings suggest that, on the contrary to the traditional view, PGE(2) functions as a mediator of immune inflammation. Consistently, administration of an EP4 antagonist could suppress disease progression and development of antigen-specific Th17 cells in mice subjected to experimental allergic encephalomyelitis and contact hypersensitivity. In this perspective, we review these findings and discuss the prospect of EP4 antagonists as immunomodulatory drugs.
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PMID:Prostaglandin E2, an immunoactivator. 2005 52