Aluminum Hydroxide Gel Adjuvant Research Articles

Protection against Schistosoma mansoni achieved by immunization with sonicated parasite.

Partial protection of (C57BL/6 X DBA/2)F1 mice against infection with Schistosoma mansoni has been achieved by immunization with small amounts (0.2 to 2.0 microgram) of crude cercarial sonicate adsorbed on aluminium hydroxide gel adjuvant (alum). A decrease of 34-90% in the adult worm burden, of the immunized mice, as compared to that of untreated mice or those injected with adjuvant alone, has been found in five experiments by liver perfusion six weeks after percutaneous challenge infection. High titers of anti-cercarial IgE antibodies have been found in the sera of the immunized mice by two independent techniques, radioimmunoassay and degranulation of rat basophilic leukemia cells (RBL-2H3), determined by 3H-serotonin release. By counting the live worms in the lungs of immunized and uniummized mice on days 4-7 after infection it was observed that the schistosomula were killed before they reached the lungs, probably at the skin. Mice immunized with the same amounts of cercarial antigen in Freund's complete adjuvant were not protected against infection with S. mansoni. These animals developed high titer of total anti-cercaria antibodies (determined by radioimmunoassay) but had low levels of antiparasite IgE. The possible role of IgE in protective immunity is discussed.

A serological comparison of Pasteurella haemolytica vaccines containing different adjuvants

Five adjuvants were compared for their ability to enhance the serological response of sheep to capsule extract of Pasteurella haemolytica biotype A serotype 6. Vaccines of this antigen were inoculated with incomplete Freund's adjuvant, complete Freund's adjuvant, incomplete Freund's adjuvant containing a water soluble extract of Mycobacterium tuberculosis, aluminium hydroxide gel or a combination of aluminium hydroxide gel and incomplete Freund's adjuvant. This latter vaccine induced significantly higher titres of antibody as measured by an indirect haemagglutination test than did any of the other vaccines. The aluminium hydroxide gel alone was shown to be the poorest adjuvant. The local reactions at the sites of inoculations produced by the aluminium hydroxide gel in incomplete Freund's adjuvant vaccine were not severe and were not detectable beyond one month after vaccination in the majority of the sheep.

Isolation of a protective, non-toxic capsular antigen from Pasteurella multocida, types B and E

Separation of the capsular antigen and endotoxin from saline extracts of Pasteurella multocida type B was achieved by fractional precipitation from aqueous solution by addition of polar organic solvents. Biological tests for the presence of endotoxin showed that it was absent from capsular antigen preparations so obtained. Properties of the capsular antigen suggested that it was a high molecular weight acidic polysaccharide. The solvent fractionation method was found to be equally applicable to separation of capsular antigen and endotoxin of P multocida type E. The type B capsular antigen in the presence of aluminium hydroxide gel adjuvant, was poorly immunogenic in rabbits. In cattle, however, a dose-dependent serological response was obtained as demonstrated by the mouse passive protection test.

Electrophoretic and Antigenic Analysis of Mouse and Guinea Pig Anaphylactic Antibodies

Abstract Mice and guinea pigs were immunized with dinitrophenyl (DNP) protein complexes in low doses combined with aluminium hydroxide gel adjuvant. This scheme led to the production of two different types of antibodies mediating passive cutaneous anaphylaxis (PCA) reactions in each species. Both species made a heat stable IgG1 antibody capable of giving PCA reactions with a short sensitization period, which was removed by treatment with specific anti-IgG1 serum, and migrated electrophoretically with the total IgG1 globulins of each species. The other antibody provoking PCA reactions in each species was detected with a longer sensitization period (2 days in mice and 4 days in guinea pigs). These antibodies did not show identical properties to each other. The mouse antibody was completely heat labile, was not removed by a specific anti-IgG1 serum, and migrated electrophoretically slightly more slowly than did IgG1. In distinction, the guinea pig antibody was only marginally affected by heating, was removed by pretreatment with a specific anti-IgG1, and had a faster electrophoretic mobility than IgG1 globulin. These results support a previous observation of Parish, that guinea pigs may possess two heat stable IgG1-type antibodies that can mediate PCA, possibly as well as having a true reaginic antibody.

Immunological Studies with Corynebacterium pyogenes in Mice

Vaccination of mice with formolised cells and toxoid prepared from Corynebacterium pyogenes, plus either Freund’s or aluminium hydroxide gel adjuvant or with a vaccine prepared from infected mouse tissues, failed to produce a high level of immunity to experimental challenge with the homologous strain. Using a live vaccine of virulent C. pyogenes, it appeared that only those mice which received a dose of vaccine sufficient to produce abscess formation developed a demonstrable degree of immunity to subsequent challenge, and even then the immunity was not of a high order. It is concluded that the possibility of successfully immunizing animals against C. pyogenes is remote.

Immunologic Studies of Heart Tissue

Summary Rabbits given repeated injections of beef or rat heart homogenates in aluminum hydroxide gel adjuvant developed focal cardiac lesions associated with antibodies to heart. The lesions were characterized by myocardial cell necrosis or degeneration with infiltration of mononuclear and polymorphonuclear cells, among which eosinophils were frequently prominent. Myocardial lesions of varying severity were observed in 7 of 9 animals injected with beef heart and 6 of 12 animals injected with rat heart. An extensive myocardial degeneration and fibrosis was observed rarely. In 13 control rabbits injected with human γ-globulin in adjuvant, these scattered focal lesions were not observed. The incidence and severity of cardiac lesions could not be related to the titer of antibodies to heart as measured by complement fixation or immunofluorescence, or necessarily, to presence of flocculating antibodies. Bound γ-globulin was detected within cardiac myofibers in focal sites of myocardium in several animals of the experimental groups, but not in the control animals. The sparseness of such deposits of bound γ-globulin in myocardium of most of the experimental animals, despite the presence of circulating antibodies to heart, suggested that impermeability of myofibers to antibody may represent a limiting factor in the pathogenesis of these lesions.