Related Experiment Video
Updated: Oct 15, 2025

09:01
Chronic Salmonella Infected Mouse Model
Published on: May 31, 2010
17.6K
Revisiting Persistent Salmonella Infection and the Carrier State: What Do We Know?
Neil Foster1, Ying Tang2, Angelo Berchieri3
1SRUC Aberdeen Campus, Craibstone Estate, Ferguson Building, Aberdeen AB21 9YA, UK.
Pathogens (Basel, Switzerland)
|October 23, 2021
Summary
Salmonella enterica serovars causing typhoid-like illness can lead to persistent infections in some individuals. These bacteria persist in macrophages, potentially by altering host immune responses.
Area of Science:
- Immunology
- Microbiology
- Infectious Diseases
Background:
- Salmonella enterica serovars causing typhoid-like infections can establish persistent infections in a subset of individuals.
- Intermittent shedding of these bacteria post-convalescence is a key epidemiological factor.
- Chronic infection persists despite high levels of specific IgG antibodies.
Purpose of the Study:
- To review the mechanisms underlying persistent Salmonella infections.
- To explore the role of host-pathogen interactions in Salmonella persistence.
- To identify potential therapeutic strategies for persistent Salmonella infections.
Main Methods:
- Literature review of Salmonella persistence studies.
- Analysis of Salmonella serovars including S. Typhi, S. Dublin, S. Gallinarum, S. Pullorum, S. Abortusovis, and S. Typhimurium in mice.
- Examination of host immune responses and macrophage polarization.
Main Results:
- Persistence of Salmonella appears to occur within macrophages in the spleen and liver.
- Shedding can originate from the gallbladder, gut, or reproductive tract.
- Salmonella modulates host immune responses from Th1 to Th2 or anti-inflammatory types and promotes M1 to M2 macrophage polarization.
Conclusions:
- Host genetic background influences Salmonella persistence.
- Bacterial modulation of host immune responses and macrophage polarization are key to persistence.
- Cytokine therapy may offer a potential strategy to restore Th1 responses and clear persistent infections.

