Biomedical subjects

C Bolton

Publications and source records attributed to C Bolton.

48 records · Page 3Linked to original sources

PubMed1985

Correlation between prostaglandin and thromboxane levels and clinical signs in cyclosporine A-treated guinea pigs with acute experimental allergic encephalomyelitis.

Prostaglandin E, prostaglandin F2 alpha and thromboxane B2 levels were measured in the spinal cord and cerebellum of guinea pigs with acute experimental allergic encephalomyelitis treated with Cyclosporine A in a schedule which delayed the onset of the disease and completely suppressed it in 40% of the animals. A correlation was found between the eicosanoid levels in the central nervous system and clinical signs of the disease. Where lesions were completely suppressed the levels of eicosanoids were normal. The number of lesions found correlated well with the clinical state of the animals.

Animals↗

PubMed1984

Prostaglandin and thromboxane levels in central nervous system tissues from rats during the induction and development of experimental allergic encephalomyelitis (EAE).

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.

6-Ketoprostaglandin F1 alpha↗

PubMed1984

Prostaglandin levels in cerebrospinal fluid from multiple sclerosis patients in remission and relapse.

Radioimmunoassay (RIA) techniques have been employed to determine prostaglandin (PG) levels in the cerebrospinal fluid (CSF) from multiple sclerosis (MS) patients in remission and relapse and in subjects with other neurological diseases (OND). PGE and PGF2 alpha concentrations in spinal fluid from MS patients in relapse were significantly lower than values estimated during remission and in individuals with OND of the central nervous system (CNS). These observations are discussed in relation to the clinical state of patients with demyelinating disease together with a consideration of the concept that disordered immune mechanisms contribute a central role in the pathogenesis of MS.

Dinoprost↗

PubMed1984

A longitudinal study of the prostaglandin content of central nervous system tissues from guinea pigs with acute experimental allergic encephalomyelitis (EAE).

The levels of prostaglandins (PGs) E, F2 alpha and 6-oxo-PGF1 alpha, in spinal cords and cerebellums of guinea pigs were measured during the development of experimental allergic encephalomyelitis (EAE). The earliest change observed was an elevation of PGE in spinal cords, but not cerebellums , 5-7 days post-inoculation (PI) and prior to the appearance of clinical symptoms. PGE content of spinal cords continued to rise until days 12-14 PI when the animals displayed paralytic EAE. In contrast, PGF2 alpha and 6-oxo-PGF1 alpha levels in spinal cords peaked on days 9-11, when the animals exhibited initial clinical signs, but fell to lower values by days 12-14 PI. In cerebellums , the PGE content increased more slowly than in spinal cords, consistent with the lower numbers of mononuclear cell infiltrates, whereas PGF2 alpha and 6-oxo-PGF1 alpha levels remained unaltered. The relationships between the observed changes in prostanoid levels, lesion development and the appearance of clinical symptoms are discussed.

6-Ketoprostaglandin F1 alpha↗

PubMed1982

Immunosuppression by cyclosporin A of experimental allergic encephalomyelitis.

Cyclosporin A (CsA), an immunosuppressant which acts selectively on antigen-responding T cells, was tried in the treatment of experimental allergic encephalomyelitis (EAE). The drug was highly effective in preventing the appearance of clinical and pathological signs of EAE in rats, guinea pigs and monkeys. Treatment of the established disease also reduced the incidence and severity of symptoms, and significantly reduced the number of inflammatory lesions in the central nervous system.

Animals↗

PubMed1982

The effect of cyclosporin A on the adoptive transfer of experimental allergic encephalomyelitis in the Lewis rat.

Experimental allergic encephalomyelitis (EAE) can be adoptively transferred in Lewis rats with spleen cells from immunized animals, after culture with concanavalin A or myelin basic protein (MBP). The effect of the immunosuppressive drug cyclosporin A (CsA) on the in vitro and in vivo steps of the cell transfer has been investigated. Clinical signs of EAE were completely suppressed by CsA in rats immunized with MBP in Freund's complete adjuvant and spleen cells from these animals, cultured with the antigen, did not transfer the disease. The incidence of transferred disease was also reduced, if recipients were treated with CsA, although a higher dose of drug than that needed to suppress active EAE was required. In both instances complete suppression of EAE was only accomplished for the period of dosing, although the clinical signs of disease which appeared after withdrawal of the drug were significantly reduced in severity. These results imply that an immune response in the host animal is a prerequisite for adoptive transfer of EAE or suggest that CsA can regulate the action of lymphocytes already primed.

Animals↗

PubMed1971