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PubMed1954

A study of the chemical nature of components of bovine white matter effective in producing allergic encephalomyelitis in the rabbit.

Fractions of bovine white matter, prepared by the methods of Folch and Lees, were studied for chemical composition and for their ability to produce experimental allergic encephalomyelitis in rabbits. Evaluation of the disease and of the lesions in animals injected with the more active fractions at several dose levels permitted comparison of the antigenic activity of these materials. When tissue was fractionated by the methods of Folch and Lees, antigenic activity was found in the chloroform-methanol extract but not in the denatured tissue residue. This activity was traced to proteolipides A and B and to the lower phase, more specifically the ether-soluble fraction of the lower phase. Proteolipide C was inactive. Correlation of the chemistry of fractions with their antigenic activity suggested two possibilities: (a) that there might be two antigens, one proteolipide and the other non-proteolipide; or (b) that a small specific proteolipide is responsible for all the observed activity. The high concentration of acetal phosphatide in the ether-soluble lower phase suggested that compounds of this type might be the hypothetical non-proteolipide antigen, but this hypothesis was disproved by analytic study of active and inactive materials. The possibility that proteolipide might account for all the antigenic activity was strongly supported by the experimental finding that total lipide and proteolipide progressively lost activity as proteolipide was degraded by adequate processing. The use of an entirely different method for preparing total lipides free of proteolipide (the colloidal iron technique) indicated that this loss of activity did not result from incidental removal of some non-proteolipide antigen. These tentative conclusions are in agreement with those of Tal and Olitsky and provide a satisfactory interpretation of the findings of Goldstein et al. The very fact, however, that the suggested proteolipide antigen would amount to no more than 1 per cent of the total chloroform-methanol extractives leaves open the possibility that some unrecognized trace substance may be the antigen. Skin tests with the various fractions indicated some cross-reactivity between proteolipides A and B and the ether-soluble lower phase fraction and a fair correlation of positive skin reactions with disease. This finding is compatible with the suggestion that the same antigen is present in both of these types of material. When the disease produced by whole tissue or fractions was evaluated by the use of the proportion of animals developing disease, the day of onset, and the severity of the histologic lesions, it was found that fractions produced milder disease of later onset than intact tissue at all dose levels. The disease-producing activity was not enhanced by increasing the dose; i.e., it appeared to reach an asymptotic maximum below that obtainable with whole fresh tissue. This finding suggests both a quantitative loss of activity and a qualitative change during the initial chloroform-methanol extraction, a procedure which denatures all proteins in the tissue residue. A comparable change appeared to occur in whole white matter stored at -15 degrees C. for 15 months and thawed and refrozen several times during this period. The later fractionation steps resulted in no apparent loss of antigenic activity. A scoring method employing the same type of data to estimate the actual relative antigen contents of different preparations is presented in the Appendix.

Animals↗
PubMed1957

Effect of nutrition on the production of acute disseminated encephalomyelitis in mice.

The susceptibility of homozygous BSVS mice to acute disseminated encephalomyelitis (ADE) has been found to be nutritionally dependent. On a laboratory stock regimen of commercial fox chow pellets, whole wheat bread, and milk this genotype is 100 per cent susceptible to the disease. On a "synthetic" diet, containing a minimal list of vitamins adequate for growth and maintenance, susceptibility was found to be reduced to 15 per cent. Supplementation of the "synthetic" diet with biotin, folic acid, and vitamin B(12) restored susceptibility to a frequency of 70 per cent. Increasing the supplements tenfold had no further effect in restoring susceptibility frequencies to the 100 per cent level. In the restoration of susceptibility, folic acid and vitamin B(12) were equally effective as single supplements and equivalent to the triple vitamin supplement. The effect of single biotin supplementation was less. An outbreak of fatal pasteurellosis among BSVS mice latently infected with Pasteurella and used in an ADE susceptibility test has been described. The fatal pasteurellosis has been ascribed to a constellation of determinants including (a) diet, (b) sex, (c) inoculation events, and (d) latent infection with Pasteurella. With males the susceptible sex it was possible to avert the fatal pasteurellosis and continue the nutritional experiments by using females exclusively.

Animals↗
PubMed1960

Transfer of allergic encephalomyelitis in rats by means of lymph node cells.

Transfer of allergic encephalomyelitis has been accomplished by injection of lymph node cells, obtained from donor rats sensitized to spinal cord, into recipient rats pretreated neonatally with normal rat spleen cells. Transfer of the disease may be achieved most frequently when the recipients are pretreated with spleen cells of the prospective lymph node cell donors. These transfers are attributed to the use of recipients which have acquired immunological tolerance to donor lymph node cells, as a result of the spleen cell pretreatment, and in which, therefore, the donor cells can survive and function longer after transfer.

Animals↗
PubMed1960

Suppression of experimental "allergic" encephalomyelitis in guinea pigs by encephalitogenic proteins extracted from homologous brain.

The intradermal injection of aqueous solutions of certain homologous neural proteins will suppress the encephalomyelitis which is induced in guinea pigs by the previous injection of whole homologous brain with Freund's adjuvants. These neural proteins extracted by dilute acid from defatted guinea pig brain are themselves highly encephalitogenic when injected with adjuvants, but the specificity of this suppression for encephalitogenic as compared to non-encephalitogenic extracts remains to be proven. Suppression is probably not due to a non-specific stress reaction, as indicated by the absence of suppression by intradermal injections of alcohol and by statistically insignificant and inconstant effects of similar injections of tuberculin.

Adjuvants, Immunologic↗
PubMed1962

Critical relationships between constituents of the antigen-adjuvant emulsion affecting experimental allergic encephalomyelitis in a completely susceptible mouse genotype.

The production of EAE in the fully susceptible BSVS mouse genotype has been found to be dependent on the ratio of proteolipid antigen and adjuvant mycobacterial concentration as used in the emulsion, of the Freund type. Disturbance of this ratio, by manipulation of either component, by diminution or increase, results in a decrease in the frequency by which EAE is produced. Simultaneous reduction of antigen and mycobacteria, so that the ratio remains unchanged, retains the full EAE-producing power of the emulsion. The limit of this has not been ascertained. Emulsifying agents have been found to restrict further the permissible limits of the antigen-mycobacterial ratio for full EAE production. Such effects of the emulsifier have been found to vary with the qualitative nature of the emulsifier. Aquaphor has been found to be less restrictive than falba. These phenomena, systematically analyzed here for the mouse, may have an application for other antigen-adjuvant systems and for other hosts.

Adjuvants, Immunologic↗
PubMed1962

Adjuvant-antigen relationships in the production of experimental "allergic" encephalomyelitis in the guinea pig.

Quantitative relationships between the amounts of encephalitogenic neural tissue and mycobacterial adjuvant are presented for the guinea pig, for comparison with similar results obtained in the mouse and presented in an accompanying paper by Lee and Schneider (27). Definite threshold amounts of both neural encephalitogenic and mycobacterial adjuvant can be defined. With the proper amounts of each component, 100 per cent of guinea pigs can be made to develop EAE, 97 per cent dying of it, and over 50 per cent becoming paralyzed by the 12th day after challenge. With moderate amounts of encephalitogen the severity and incidence of EAE can be very great, but this encephalitogenic potential can be masked if large amounts of mycobacteria are employed. The mechanism of this masking effect by excess adjuvant is not known, but speculation centers upon the possibility of competition of antigens of the mycobacteria at the expense of those of the encephalitogen.

Adjuvants, Immunologic↗
PubMed1962

Prevention of experimental allergic encephalomyelitis (EAE) by vitamin C deprivation.

Scorbutic guinea pigs injected with CNS and mycobacterium to induce experimental allergic encephalomyelitis (EAE) showed no clear-cut neurological signs and failed to show histological evidence of central nervous system damage. The degree of protection afforded by vitamin C deprivation was related directly to the duration of the scorbutogenic diet and inversely to the strength of the CNS challenge. Vitamin C deprivation also abolished tuberculin sensitivity as measured by the PPD skin reaction. Upon restoration of vitamin C, the animals recovered their sensitivity to PPD but did not develop EAE. It was further demonstrated that these effects of vitamin C deprivation were not related to inanition or to the endogenous levels of 17-hydroxycorticosteroids.

Animals↗
PubMed1962

The encephalomyelitic activity of myelin isolated by ultracentrifugation.

A relatively simple preparation of guinea pig brain myelin, free of gross contamination by other cellular elements has been described. Electron microscopic evidence of the predominance of membranous (lamellar) forms was used as the criterion of purity of this fraction. The slight mitochondrial contamination of the myelin fraction was confirmed by its low succinic dehydrogenase activity. Quantitative bio-assay of the encephalitogenic activity of myelin showed it to have a higher specific activity than whole guinea pig brain. The low encephalomyelitic activity of the other subcellular constituents (nuclei and mitochondria) which were removed from myelin by ultracentrifugation in 30 per cent sucrose could be explained by a small amount of myelin contamination. A basic protein of high specific encephalitogenic activity has been isolated from myelin by methods previously applied to whole brain. Although the protein is similar to nuclear histones, the following facts point to certain significant differences. Nuclei prepared by a different procedure from the one developed for the isolation of myelin were found to be non-encephalitogenic. Although basic protein could be extracted readily from these nuclei by dilute HCl, the same extraction procedure yielded little extractable protein from whole myelin. Myelin which had been defatted by cold chloroform-methanol yielded a basic protein which was highly encephalitogenic. The evidence presented thus supports the view that there exists in myelin a new basic protein responsible for the induction of experimental allergic encephalomyelitis, which is distinctly different from nuclear histones. The possible relationship of this protein to myelin structure and function has been discussed.

Animals↗
PubMed1962

Experimental allergic encephalomyelitis: the effect of 6-mercaptopurine.

1. 6-Mercaptopurine (6-MP) prevents experimental allergic encephalomyelitis (EAE) during the period of drug administration in both rabbits and guinea pigs. The disease is suppressed even when treatment is started as late as the 5th day after antigenic stimulation in guinea pigs and the 12th day in rabbits. 2. After discontinuation of 6-MP treatment, there is a latent period before the disease is noted. The length of this latent period is not modified by the duration of 6-MP treatment. 3. The effect of 6-MP on EAE is not the result of leukopenia, non-specific toxicity and debilitation, anti-inflammatory activity, or mere masking of clinical signs of the disease. It is, rather, the result of 6-MP's specific anti-immunologic activity. 4. The effects of 6-MP on antibody production, delayed hypersensitivity, and EAE are compared. This provides indirect evidence for the importance of circulating antibody in the pathogenesis of EAE. 5. The important considerations in the use of 6-MP are discussed and the possible usefulness of 6-MP in human neurologic diseases is considered.

Animals↗
PubMed1953

An antiviral substance from Penicillium funiculosum. I. Effect upon infection in mice with swine influenza virus and Columbia SK encephalomyelitis virus.

A culture of P. funiculosum isolated on Guam proved capable of elaborating a substance which exerted a favorable therapeutic effect against swine influenza virus infections in white mice. The culture was extremely variable and irregular in its production of the antiviral substance, and during maintenance in the laboratory for several years gradually lost this property. Efforts to restore it were unsuccessful. Subsequently it was found that the mold elaborated a substance, now designated helenine, which is therapeutically effective against Columbia SK encephalomyelitis virus infections in mice. Helenine appears to differ from the substance earlier procured from the mold, which was active against swine influenza virus infections in mice. It is frequently present in greater or lesser amount in the fluid portions of stationary cultures of P. funiculosum but is more regularly obtained and in larger amount, from the cellular components of the pellicles. When liberated from these latter by mechanical bruising and fracturing, it goes into solution in the culture fluids. It is precipitable from aqueous solution by 50 per cent acetone. Infected mice injected with helenine in amounts less than the amount which produces a maximal therapeutic effect exhibit a dosage response. Increasing the dose above the optimum fails to increase the therapeutic effect. Helenine exerts its maximum effect when given within the first 10 hours after viral infection but its influence is apparent even when treatment is delayed for up to 24 hours. It is not effective against massive amounts of virus and gives the best therapeutic results when used in the treatment of animals infected with from 10 to 1000 fatal doses of virus. Treatment of infected mice with helenine delays the entrance of virus into their brains for from 24 to 48 hours. The mechanism by which helenine exerts its therapeutic effect against SK virus is not known but the findings presented suggest either that it causes an inhibition or interruption of multiplication of the virus, slowing down the whole process of infection and spread to the central nervous system, or that in some way it interferes temporarily with the neuroinvasiveness of the virus.

Animals↗
PubMed1953

Inhibition of Theiler's encephalomyelitis virus (GDVII strain) of mice by an intestinal mucopolysaccharide. I. Biological properties and mechanism of action.

A mucopolysaccharide has been obtained from intestinal tissue of adult mice which inhibits both infectivity and hemagglutination of Theiler's GDVII strain of encephalomyelitis virus of mice. The inhibitor is inactive against the FA and TO strains of Theiler's virus and against the Lansing strain of poliomyelitis virus. In the adult mouse, large amounts of the inhibitor are found only in the small intestine. The small intestine of infant mice, however, contains a considerably smaller amount of inhibitor. Inhibition, both in vivo and in vitro, appears to be the result of an interaction between virus and inhibitor. The intestines of man, monkey, rabbit, rat, cotton rat, hamster, sheep, cow, and pig contain relatively little inhibitor whereas guinea pig intestine contains as much as adult mouse intestine. An enzyme was found in the feces of mice, and several other animals, which is capable of destroying the inhibitory activity of the mucopolysaccharide with the liberation of reducing sugars.

Animals↗
PubMed1953

Inhibition of Theiler's encephalomyelitis virus (GDVII strain) of mice by an intestinal mucopolysaccharide. II. Purification and properties of the mucopolysaccharide.

A mucopolysaccharide inhibitor of Theiler's GDVII virus has been purified from intestinal tissue of adult mice. The purified material has been shown to consist chiefly of carbohydrate. Following acid hydrolysis of the inhibitor, several amino adds were found to be present. The carbohydrate components shown to be present thus far are galactose, hexosamine, N-acetylhexosamine, methylpentose, hexurornic acid; an indication has been obtained that sedoheptulose is also present. The available evidence strongly suggests that this mucopolysaccharide, and not some other substance present in minute amounts, is the inhibitor of the GDVII virus.

Animals↗
PubMed1953

Susceptibility of mice free of Theiler's virus (TO strain) to infection with TO virus.

A method for the establishment and maintenance of a colony of mice free of Theiler's (TO) virus has been described. This colony has been maintained since 1947 with but one instance of contamination in 1948. Studies on the susceptibility of these mice to TO virus show that smaller doses are required to establish an infection of the intestinal tract than of the CNS. A mutant strain of TO(B) virus has been isolated which, following oral administration to mice free of TO virus, is able to cause infection of the CNS with paralysis. When fed to stock mice that carry TO virus, this TO(B) strain does not cause paralysis or other signs of CNS infection.

Animals↗