PubMed Health⌕ Search

Biomedical subjects

A J Suckling

Publications and source records attributed to A J Suckling.

At least 37 records · Page 2Linked to original sources
PubMed1983

Chronic relapsing experimental allergic encephalomyelitis. The presence in the cerebrospinal fluid of factors chemotactic for monocytes.

Cerebrospinal fluid (CSF) was removed from guinea pigs with chronic relapsing experimental allergic encephalomyelitis (CR-EAE) and control inoculated animals by puncture of the cisterna magna. The fluid from 7/8 animals in relapse and 2/4 animals in remission phases of CR-EAE was found to promote the migration of peripheral blood monocytes through a 5-micron pore diameter polycarbonate membrane filter. Monocytes were also found to orient towards the migration-stimulating CSF in a gradient formed between such fluid and CSF derived from a control animal, thereby indicating the presence of a chemotactic factor. The factor responsible for promoting monocyte migration had a molecular weight of between 50 000 and 300 000 as defined by ultrafiltration. The results are discussed in relation to the known pathohistological features of the chronic relapsing disease.

Animals↗
PubMed1983

Chronic relapsing experimental allergic encephalomyelitis. Immunological and blood--cerebrospinal fluid barrier-dependent changes in the cerebrospinal fluid.

Cerebrospinal fluid (CSF) and plasma were taken from strain 13 guinea pigs in various stages of chronic relapsing experimental allergic encephalomyelitis using techniques which allowed repeated sampling from the same animal. Samples were assayed for albumin and IgG and the corresponding CSF/plasma quotients evaluated graphically using a method which could discriminate between blood-CSF barrier dysfunction and local IgG synthesis in the central nervous system (CNS). During the disease a 2-3-fold increase in plasma IgG concentration developed and an increase in blood-CSF permeability was noted. Isoelectric focusing revealed an oligoclonal IgG pattern identical in both plasma and CSF. The results provided no evidence for a local production of IgG in the CNS like that which is known to occur in multiple sclerosis.

Albumins↗
PubMed1982

Immunoglobulin synthesis in nude (nu/nu), nu/+ and reconstituted nu/nu mice infected with a demyelinating strain of Semliki Forest virus.

Infections with the avirulent (A7/74) strain of Semliki Forest virus which causes primary demyelination of the central nervous system in mice have been studied further in nude athymic (nu/nu) mice and their immunocompetent (nu/+) litter mates to measure the production of immunoglobulins. This has been done by radial immunodiffusion and enzyme-linked immunosorbent assays. Half the nude mice examined were able to synthesize specific IgG but at levels 1,000-fold lower than their nu/+ littermates. The majority of nude mice reconstituted with spleen cells from nu/+ mice 1 day before infection with virus were able to synthesize specific IgG nearly as well as the nu/+ animals.

Animals↗
PubMed1980

The effect of mouse strain on the pathogenesis of the encephalitis and demyelination induced by avirulent Semliki Forest virus infections.

Mice from the following strains--Simpson, SWR/J, TO, CBA/Ca, CW (outbred), LAC/G (outbred), SJL/J and Swiss A2G (outbred)--were infected i.p. with avirulent Semliki Forest virus. Clinical signs of disease were noted, histopathological changes assessed and the blood and brain virus infectivities and serum immunoglobulin levels were measured. Only the CW, TO and Swiss/A2G animals showed convincing evidence of demyelination at the light microscopy level but all strains developed encephalitis and microcystic (spongiform) lesions.

Animals↗
PubMed1978

Virus-associated demyelination. A model using avirulent Semliki Forest virus infection of mice.

Lesions produced by the infection of Swiss/A2G mice with a single inoculation of an avirulent strain of Semliki forest virus have been studied by light and electron microscopy. Whilst a mild encephalitis was detected in the great majority of mice infected, focal areas of myelin loss were observed in the cerebellar white matter of only 25% of cases. The incidence of myelin loss in other strains of mice ranged from 21% in BSVS mice to 8% in SJL/J mice. The possible mechanisms involved in the pathogenesis of the myelin loss are discussed.

Animals↗
PubMed1978

The pathogenesis of avirulent Semliki Forest virus infections in athymic nude mice.

The course and outcome of intraperitoneally induced infections with the avirulent strain A7(74) of Semliki Forest virus have been studied in athymic 'nude' (nu/nu) mice, their heterozygous (nu/ + ) littermates and conventional Swiss A2G mice. The main distinguishing characteristics of the infection in the nu/nu mice were the persistence of virus in the brain after an initial phase of incomplete virus clearance and the apparent establishment of a secondary phase of virus replication in the brain which was associated with a falling neutralizing antibody response. This secondary phase of virus replication persisted until at least the 28th day after inoculation. In addition the typical histological lesions of encephalitis induced by this virus were rare and focal demyelination, which occurred at a light microscopy level in up to 26% of nu/ + and Swiss A2G mice, was not observed. It is suggested that in immunocompetent mice the development of lesions including demyelination may be a result of an immunopathological response to virus infection which is related to the presence of thymus derived lymphocytes.

Animals↗