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Updated: Jul 24, 2026

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Murine Distal Colostomy, A Novel Model of Diversion Colitis in C57BL/6 Mice
Published on: July 12, 2018
Experimental melioidosis in inbred mouse strains
D Veljanov1, A Vesselinova, S Nikolova
1Institute of Microbiology, Bulgarian Academy of Sciences, Sofia, Bulgaria.
Summary
This study shows that different mouse strains exhibit varying susceptibility to Pseudomonas pseudomallei infection. Host genetics significantly influence bacterial load and tissue damage, highlighting the importance of host-dependent responses in infectious disease.
Area of Science:
- Immunology
- Microbiology
- Genetics
Background:
- Pseudomonas pseudomallei causes melioidosis, a serious infectious disease.
- Understanding host-pathogen interactions is crucial for developing effective treatments.
- Inbred mouse strains offer a model to study genetic influences on disease severity.
Purpose of the Study:
- To investigate the susceptibility of different inbred mouse strains to Pseudomonas pseudomallei.
- To characterize the host immune response and bacterial load in various tissues.
- To determine the role of host genetics in the outcome of experimental melioidosis.
Main Methods:
- Induction of experimental infection with Pseudomonas pseudomallei in BALB/c, BDF1, and C57BL mice.
- Quantification of bacterial load in visceral organs.
- Evaluation of blood cell parameters and peritoneal exudate cells using an automated hematology analyzer.
- Histopathological examination of infected tissues.
Main Results:
- All mouse strains showed an inflammatory response with granulocyte and macrophage shifts.
- C57BL mice exhibited the highest bacterial load in the liver and spleen, correlating with severe tissue damage.
- BALB/c and BDF1 mice had lower bacterial counts and less pronounced histological changes compared to C57BL mice.
Conclusions:
- Mouse strain significantly impacts the severity of Pseudomonas pseudomallei infection.
- Host genetic factors play a critical role in determining susceptibility and disease progression.
- These findings underscore the importance of host-dependent variations in infectious disease models.

