The Chemical Compositions in the Cell Wall of Salmonella typhimurium affecting the Clearance-Rate in Mouse

Microbiology and Immunology

1980

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Treatment of mice with 0.01–1 μg of a synthetic serum thymic factor (FTS) significantly increased their resistance to lethal doses (1–5 × 106 organisms) of Salmonella typhimurium LT2 (LT2). At least seven injections of FTS were necessary for induction of resistance, since the effects of one to three injections were variable. FTS additively potentiated the protective immunity to LT2 induced by immunization with an avirulent mutant of LT2, irrespective of the structural components of the cell wall lipopolysaccharides of the mutants, which are basically correlated with their immunogenicity and virulence. Activated macrophages may have a direct role in the induction of host resistance, since peritoneal macrophages from FTS‐treated DBA/2 mice which are resistant to the doses of LT2 used could by themselves retard bacterial growth in vitro, whereas those from CBA/N mice which are relatively susceptible to LT2 did not inhibit bacterial growth without intervention of FTS‐treated syngeneic T cells.

Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Nonspecific Stimulation of Antibacterial Resistance by a Synthetic Thymic Factor (FTS) in Mice

Matsumoto

Microbiology and Immunology

1980

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“…Opsonic and bactericidal actions of antibodies are quite specific for the antigenic components of polysaccharides on the cell surfaces of the organisms (13,14). Cell-mediated protection against salmonella infection does not depend on the surface o antigenic components of the organisms (12,22).…”

mentioning

confidence: 99%

Delayed Hypersensitivity in Murine Salmonellosis: Specificity of Footpad Reaction in Mice Infected with Rough Mutants of Salmonella typhimurium

Cho

Saito‐Taki

Microbiology and Immunology

1983

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Delayed type (footpad) hypersensitivity (DTH) in BALBjc mice immunized with rough mutant strains of Salmonella typhimurium LT2 was examined. Injection of live organisms of an Rb mutant TVI48 strain induced DTH in mice, while injection of the heat-killed organisms did not. The mice immunized with live organisms of the Ra, Rb, Rc, Rd, and Re mutant strains showed positive footpad reactions to the heat-killed cell antigen of LT2 (wild type) strain. The mice immunized with the Rb mutant strain also showed positive footpad swellings in response to heat-killed cell antigens of S. paratyphi A, S. paratyphi B, S. typhi, S. enteritidis, and S. cholerae-suis. Furthermore, positive reactions to antigens of Escherichia coli and Shigella jlexneri were seen in the TVl48-immunized mice, but the mice did not respond to heat-killed organisms of Pseudomonas aeruginosa or Staphylococcus aureus. The crossreactive footpad reaction to E. coli could be transferred adoptively with T cells prepared from the spleens of TV I48-immunized mice into syngeneic recipients. These results suggest that the cross-reactive DTH antigen(s) is widely distributed among related organisms such as Shigella and Escherichia.

“…Virulent wild-type S. typhimurium LT2 and derived attenuated rough mutant strains TV119 and SL1004 were used. Origin, characteristics, virulence and immunogenicity of these bacterial strains were reported elsewhere [23,24]. Bacterial suspensions were prepared in saline from an 18 hr culture on Difco nutrient agar, and 0.2 ml of the suspension was injected into mice intraperitoneally (ip) or intravenously (iv).…”

Section: And K Saito Materials and Methodsmentioning

confidence: 99%

Antibody Formation in Mice Infected with Salmonella typhimurium by Primary Immunization with Sheep Erythrocytes or Bacterial Cells

Japanese Journal of Microbiology

Saito

1970

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Infection of mice with a strain of Salmonella typhimurium, known to multiply in macrophages, resulted in a marked alteration of their antibody response to further antigenic stimulation with sheep red blood cells (sRBC) or killed bacterial cells. The mice infected with a wild-type S. typhimurium and simultaneously immunized with sRBC, showed a significantly stimulated immune response to sRBC as revealed by the increased number of hemolytic plaque-forming cells in their spleens during the period following such immunization. Whether the animals were infected intraperitoneally or intravenously did not affect the stimulant effect of the infection on the immune response to sRBC. Injection of killed bacteria in amounts up to 106 organisms, instead of infection with live organisms, did not elicit any effective enhancement of antibody formation to sRBC. In cases of attenuated S. typhimurium infection, the stimulant effect on antibody formation to sRBC was obvious in the mice infected with the organisms simultaneously with or 1 week prior to the sRBC injection, while a slight suppression of antibody formation was observed in mice infected 3 weeks before the injection with sRBC. A similar effect of the infection was observed when the serum anti-bacterial antibody response was examined after stimulation with bacterial antigens. The altered immune responses after Salmonella infection are discussed in relation to the adjuvant effect of bacterial endotoxins and also to the acquired immunity to mouse typhoid.