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The effect of sodium hyaluronate on phagocytosis was studied using a sensitive polystyrene latex sphere assay in mouse peritoneal macrophage monolayers. Viscous solutions of high molecular weight hyaluronate (4.6 × 105-2.8 × 106) caused a dose-dependent inhibition of phagocytosis, but low molecular weight hyaluronate (9.0 × 104) was not inhibitory at equivalent viscosity. The inhibitory effect of high molecular weight hyaluronate did not appear to be mediated by the polyanionic charge of the molecule since sulphated glycosaminoglycans with greater charge density (heparin and chondroitin sulphate) were ineffective. In addition, competitive inhibition studies indicated that a direct effect on possible cell surface membrane receptors was unlikely. Instead, physical factors such as steric hindrance by the continuous polymeric network, were considered of more importance. Alternatively, the hydrophilic polysaccharide may have inhibited phagocytosis by providing an unsuitable surface for adhesive contact between the latex beads and the cell surface. [ABSTRACT FROM AUTHOR]

The immune responsiveness of mice infected with 90 cercariae of Schistosoma mansoni has been investigated Post-infection kinetics of antibody responses, delayed hypersensitivity and mitogen responsiveness show that there are profound disturbances of these immunological parameters starting 2 weeks after the refection. Although the final outcome is immunodepression the S. mansoni infection can produce immunostimulation. We have observed differences in the kinetics of the depression of humoral antibody responses in two strains of mice. It seems that the worms and not the eggs are of major importance in determining the observed alterations of immune responsiveness. [ABSTRACT FROM AUTHOR]

With the use of chopped guinea-pig lung, previously perfused with Tyrode's solution, the rate and extent of uptake of antibody λ globulin has been measured using “131”I-labelled rabbit antibody. The reversibility of uptake was studied by soaking the tissue in Tyrode's solution or in a solution of unlabelled λ globulin. Uptake and wash-off of antibody resembled a process of reversible adsorption, and occurred both at low temperatures and when dead tissue was used. Wash-off of labelled antibody was more rapid in the presence of added normal rabbit λ globulin than in its absence. Simultaneous measurements were made of the degree of sensitization, defined as the ability of the tissue to release histamine on subsequent contact with antigen for a standard period of time at 37°. It was found that a plateau level of sensitization had been reached in a few minutes, when only a small fraction of the total antibody eventually taken up had been adsorbed. Under the conditions of our experiments, it was not possible to wash off the antibody sufficiently to de-sensitize the tissue. Evidence was obtained that antigen was most effective in releasing histamine when added over a broad but definite range of antigen excess. By pre-incubation of the labelled antibody with lung tissue, or by ‘screening’ in a living guinea pig, it was shown to be unlikely that sensitization was due to taking up by the lung of a specific readily adsorbed fraction of antibody. When the antibody preparation was separated by chromatography into physico-chemically distinct fractions, there were quantitative differences, but all were taken up and caused sensitization of the tissue. The mechanism of sensitization of guinea-pig lung by rabbit antibody is discussed, and is considered to be one of reversible adsorption of λ globulin at unidentified sites. [ABSTRACT FROM AUTHOR]

The methods successfully used to induce immunological tolerance in mice to a variety of antigens were applied to studies on mycobacterial antigens (whole tubercle bacilli). Mice were injected with approximately 5 × 105 living attenuated (BCG) or heat-killed virulent (H37Rv) tubercle bacilli on the 15th, 16th or 17th day of foetal life. Acid-fast bacilli were found in the lungs, spleens and livers of these mice after birth. Such mice subsequently developed normally and were not more susceptible to BCG than mice primarily infected in adult life. The immunological state of the mice exposed to mycobacteria in utero was determined by challenging 5 to 6 weeks after birth with either virulent or attenuated tubercle bacilli. These tests showed that an intra-embryonic injection of mycobacteria resulted in protective immunity and not tolerance. Furthermore, the mice also showed delayed-type hypersensitivity to mycobacteria. These results are discussed in relation to the ability of other antigens to induce immunological tolerance in mice and to the response of other animal species to mycobacteria. [ABSTRACT FROM AUTHOR]

A state of acquired immunological tolerance to bovine gamma globulin (BGG) has been observed in CBA mice injected with 10 mg. BGG within 12 hours of birth. Tolerance was demonstrated by a lack of immune elimination of 131I labelled BGG (BGG-131I) after prior challenge with Freund's adjuvant containing BGG. The degree of tolerance was found to diminish when the time between the tolerance injection and the challenge injection with adjuvant was increased. Mice were found to be tolerant 4 months after injection of 10 mg. BGG at birth but other similarly treated mice were found to be partially immune when challenged 6 months after the tolerance injection. This diminution of tolerance could be prevented by injections of antigen into adult mice whilst they were still tolerant. Precipitin and haemagglutination tests showed that antibody to BGG was present in mice shown to be tolerant to BGG by the antigen-elimination technique. The Ouchterlony double-diffusion technique showed that the mice were tolerant to one fraction of BGG but immune to at least one other fraction. The tolerated fraction of BGG was identified by means' of starch-gel electrophoresis. [ABSTRACT FROM AUTHOR]

Immuno-conglutinin has been stimulated in rabbits after infection with Listeria monocytogenes, Salmonella typhi-murium and other bacterial species. Infection of rabbits with Western Equine Encephalomyelitis, Hammon Reeves, Murray Valley Encephalitis and Aedes trivittatus viruses also stimulated the production of this substance. The most marked immuno-conglutinin response followed infection of rabbits with Trypanosma brucei. Rickettsia burneti infection in guinea pigs produced a biphasic immunoconglutinin response, the first phase being coincident with the rise of antibodies to the Phase II antigen and the second phase with the retarded rise of antibodies to the Phase I antigen. In mice also, the immuno-conglutinin level was raised following infection with Escherichia coli, Salmonella typhi-murium and other bacterial species. [ABSTRACT FROM AUTHOR]