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At least 19 recordsLinked to original sources
PubMed1958

Tissue culture studies on bacterial allergy in experimental brucellosis. I. The effect of Brucella suis whole antigen on cultures of spleen from normal and brucella-infected guinea pigs.

Tissue culture methods have been used to investigate infectious allergy in experimental brucellosis. A study was made of the effect of whole cell Brucella antigen on cultures of spleen from normal and Brucella-infected guinea pigs. The degree of toxicity was based upon the inhibition of migration of wandering cells and upon the morphologic appearance of stained sections of tissue cultures at different periods of incubation. A suspension of heat-killed Br. suis was more toxic for splenic cells from guinea pigs infected with Br. suis than for normal splenic cells. Macrophages were more sensitive than leucocytes to the toxic action of the antigen. The degenerative changes observed in Brucella-sensitive cells exposed to the antigen were similar to the degeneration previously observed in cultures of tuberculin-sensitive cells in the presence of tuberculin. The specific toxicity of the whole Brucella antigen, however, was more marked than that of tuberculin. Preliminary experiments indicate that serum and plasma containing specific antibodies obtained from Brucella-infected guinea pigs reduce the toxic effect of the antigen in cultures of both normal and Brucella-sensitive cells. The protective action of the homologous antiserum was greater for Brucella-sensitive cells than for normal cells.

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PubMed1958

A cellular basis of immunity in experimental Brucella infection.

Brucella suis, Brucella abortus, and Brucella melitensis were shown by microscopic and cultural procedures to multiply extensively within normal rat, mouse, and guinea pig monocytes maintained in vitro in cell cultures for 3 days. Intracellular growth of brucellae had no observable toxic effects on most monocytes, although many of the cells became completely engorged with brucellae within 3 days. Non-smooth brucellae and strain 19 multiplied slowly within normal monocytes. In contrast, "immune" monocytes) i.e. those derived from animals previously infected with smooth brucellae, greatly restricted the intracellular growth of smooth and non-smooth brucellae and strain 19. Growth of smooth Brucella, within either normal or "immune" monocytes, was not influenced by addition of Brucella antiserum to the culture medium. Desensitization of immunized guinea pigs did not diminish the refractory state of their monocytes. Cellular resistance did not develop when animals were vaccinated with heat-killed brucellae, though these animals did produce agglutinating antibody. Similarly, vaccination of animals with living, rough B. suis failed to induce a refractory state in their monocytes, even though the vaccinated animals developed delayed hypersensitivity to smooth Brucella antigen. In vivo studies of Brucella survival in the spleens of normal and vaccinated mice (treated with streptomycin to prevent extracellular survival) gave strong support to the in vitro demonstrations of acquired "cellular immunity." Some implications of these results are discussed.

Animals↗
PubMed1959

Acute hepatic necrosis induced by Brucells infection in hyperthyroid mice.

When small numbers of Brucella melitensis were inoculated into ABC mice, occasional hepatic granulomas without necrosis were demonstrated. The greatest multiplication of brucellae was detected in the spleens. Because it had been previously observed that ACTH or cortisone markedly accelerated the multiplication of brucellae in the livers of infected mice with destruction of liver cells, it was considered that triiodothyronine might likewise exaggerate a brucella infection by stimulating endogenous adrenal secretion. Although adrenal hypertrophy was produced, infection of mice treated with triiodothyronine resulted in severe hepatic necrosis or infarcts without the multiplication of brucellae in either the livers or spleens. The lesions were not encountered in untreated infected mice or in control mice treated with triiodothyronine. The necrosis was associated with minimal inflammatory reaction. The necrosis was not induced in mice treated with triiodothyronine and given brucella endotoxin. The precise genesis of the acute hepatic necrosis cited in these experiments remains undefined. Triiodothyronine did not cause deaths in mice infected with Br. melitensis. The infection was neither enhanced nor suppressed.

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