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Abstract:
Salmonella is traditionally described as a facultative intracellular parasite, and host macrophages are regarded as the primary effector cells in both native and acquired immunity in mouse typhoid. This concept has not been unanimously accepted in the literature. Based on cell culture experiments and electron microscopic examinations of infected tissues, we observed that virulent Salmonella typhimurium is killed within polymorphs and macrophages of guinea pigs and mice. In a systemic disease, the organism propagates primarily in the extracellular locations of sinusoids and tissue lesions and within hepatocytes. Hence, it is more likely to be an extracellular pathogen and its virulence is directly related to its antiphagocytic property. The conspicuous absence of macrophages in the primary lesions of murine salmonellosis disputes the likelihood of their significant role in native resistance to the disease. Acquired cellular immunity is expressed as an enhanced antibacterial activity of macrophages facilitated by cytophilic antibodies rather than as an altered antibacterial action of immune macrophages. It is proposed that acquired immunity in murine salmonellosis is a synergistic manifestation of the innate capacity of polymorphs and macrophages to destroy ingested salmonellae, the activated antibacterial functions of macrophages mediated by cytophilic antibodies, the opsonic and agglutinating actions of antiserum, and the accelerated inflammation associated with delayed hypersensitivity to bacterial antigens. Unlike live attenuated vaccines, nonviable vaccines offer a significant, though not a solid, protection against subsequent challenges.
Insights
Salmonella typhimurium is primarily an extracellular pathogen, not intracellular. Its virulence stems from its ability to evade phagocytosis, challenging traditional views of macrophage immunity in mouse typhoid.
Area of Science:
- Immunology
- Microbiology
- Pathogen Biology
Background:
- Macrophages are traditionally considered key in Salmonella immunity.
- This study questions the intracellular parasite model for Salmonella.
Purpose of the Study:
- To re-evaluate the pathogenic role of Salmonella typhimurium.
- To investigate the cellular locations and immune mechanisms involved in Salmonella infection.
Main Methods:
- Cell culture experiments.
- Electron microscopic examination of infected tissues.
- Analysis of immune responses in murine models.
Main Results:
- Salmonella typhimurium is killed intracellularly by polymorphs and macrophages.
- The pathogen primarily replicates extracellularly in sinusoids, lesions, and hepatocytes.
- Virulence correlates with antiphagocytic properties, and macrophages are absent in early lesions.
- Acquired immunity involves enhanced macrophage activity via cytophilic antibodies.
Conclusions:
- Salmonella typhimurium functions as an extracellular pathogen.
- Immunity involves polymorphs, macrophages, antibodies, and hypersensitivity.
- Nonviable vaccines provide partial protection against Salmonella challenges.