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Persistent plaque formation in experimental murine brucellosis
Abstract:
Primary plaque forming cells (PFC) are present in spleens of mice 150 days or more following an infection with Brucella abortus. The development of primary plaques in mice long after antigenic challenge is an uncommon phenomenon, unlike the plaque formation (PF) induced by a non-living antigen. The mechanism of this persistent PF has been now investigated in light of a prolonged persistence of the corresponding antigen in tissues. Living E. coli, inoculated in massive dose into mice, survived in their organs for a brief time, while concomitantly PFC disappeared by day sixteen. Infection with B. abortus, in contrast, induced persistent presence of bacteria in the organs of inoculated mice and stimulated long lasting plaque formation. Only direct plaques were found during all stages of infection. Repeated inoculations of dead B. abortus also induced continuous production of primary plaques, whereas an interval in supply of the antigen resulted in disappearance of PFC. Rifampin (40 mg/kg) eliminated bacteria from the treated mice, which resulted in the disappearance of primary PFC. It seems likely that long lasting PF in B. abortus infected mice is connected with a constant antigenic stimulus operating in the carrier state.
Insights
Persistent plaque formation in mice long after Brucella abortus infection is linked to continuous antigenic stimulation. This study investigates the mechanism behind this prolonged immune response in the carrier state.
Area of Science:
- Immunology
- Microbiology
- Infectious Diseases
Background:
- Primary plaque-forming cells (PFC) typically disappear after antigen clearance.
- Prolonged immune responses after infection are uncommon, especially with persistent antigen presence.
Purpose of the Study:
- To investigate the mechanism of persistent plaque formation (PF) following Brucella abortus infection.
- To understand the role of persistent antigen in maintaining the immune response.
Main Methods:
- Comparing plaque formation after infection with live E. coli versus B. abortus.
- Administering dead B. abortus and observing PFC development.
- Using rifampin to eliminate bacteria and assess PFC persistence.
Main Results:
- B. abortus infection led to persistent bacteria and long-lasting plaque formation.
- E. coli infection resulted in transient bacteria and rapid PFC disappearance.
- Antibiotic treatment eliminating B. abortus also eliminated PFC.
- Repeated dead B. abortus inoculations maintained PFC production.
Conclusions:
- Long-lasting plaque formation in B. abortus-infected mice is associated with a constant antigenic stimulus.
- The carrier state likely maintains the immune response through persistent antigen exposure.