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Published on: October 22, 2013
A murine intraperitoneal infection model reveals that host resistance to Campylobacter jejuni is Nramp1 dependent
Olivia L Champion1, Yanet Valdez, Lisa Thorson
1University of British Columbia, Department of Microbiology and Immunology, Life Sciences Centre, 2558-2350 Health Sciences Mall, Vancouver, British Columbia V6T 1Z3, Canada.
Abstract:
We tested the hypothesis that host resistance to Campylobacter jejuni is Nramp1 dependent. Following intraperitoneal (IP) inoculation of Nramp1+/+ and isogenic Nramp1-deficient (Nramp1-/-) mice C. jejuni primarily associated with mac1-positive cells in liver tissue. A significant reduction of C. jejuni was observed in Nramp1+/+ mice 4 days post-infection (PI) (liver) and 8 days PI cecum-colon. In contrast, Nramp1-/- mice showed no significant reduction of C. jejuni and instead had a chronic inflammatory response and significant histopathological lesions 30 days PI. Differential cytokine profiles were observed in C. jejuni infected Nramp1+/+ and Nramp1-/- primary dendritic cells. Taken together these data indicate that Nramp1 is critical for host resistance to C. jejuni.
Insights
Host resistance to Campylobacter jejuni infection depends on Nramp1. Nramp1-deficient mice show increased susceptibility and chronic inflammation, highlighting Nramp1
Area of Science:
- Immunology
- Microbiology
- Genetics
Background:
- Campylobacter jejuni is a leading cause of bacterial gastroenteritis worldwide.
- Host resistance mechanisms against C. jejuni are not fully understood.
- Soluble innate immunity, including Nramp1, plays a role in controlling intracellular pathogens.
Purpose of the Study:
- To investigate the role of Nramp1 (natural resistance-associated macrophage protein 1) in host resistance to C. jejuni infection.
- To determine if Nramp1 deficiency impacts C. jejuni colonization and host immune response.
Main Methods:
- Intraperitoneal inoculation of C. jejuni in Nramp1+/+ (wild-type) and Nramp1-/- (deficient) mice.
- Quantification of C. jejuni in liver, cecum, and colon tissues at various time points post-infection.
- Histopathological analysis of infected tissues.
- Analysis of cytokine profiles in primary dendritic cells.
Main Results:
- C. jejuni primarily associated with mac1-positive cells in the liver of infected mice.
- Nramp1+/+ mice showed a significant reduction in C. jejuni load by 4 days post-infection (liver) and 8 days post-infection (cecum-colon).
- Nramp1-/- mice exhibited no significant reduction in C. jejuni, developing chronic inflammation and histopathological lesions by 30 days post-infection.
- Differential cytokine profiles were observed between Nramp1+/+ and Nramp1-/- dendritic cells upon C. jejuni infection.
Conclusions:
- Nramp1 is critical for effective host resistance against C. jejuni infection.
- Nramp1 deficiency leads to increased susceptibility, impaired bacterial clearance, and chronic inflammatory pathology.
- Nramp1 influences the immune response to C. jejuni, as evidenced by differential cytokine production.
