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A MyD88-deficient mouse model reveals a role for Nramp1 in Campylobacter jejuni infection
Robert O Watson1, Veronica Novik, Dirk Hofreuter
1Section of Microbial Pathogenesis, Yale University, School of Medicine, New Haven, CT 06536, USA.
Abstract:
Campylobacter jejuni is a major worldwide cause of enteric illnesses. Adult immunocompetent mice are not susceptible to C. jejuni infection. However, we show here that mice deficient in the adaptor protein myeloid differentiation factor 88 (MyD88), which is required for signaling through most Toll-like receptors, can be stably colonized by C. jejuni but not by isogenic derivatives carrying mutations in known virulence genes. We also found that Nramp1 deficiency increases the mouse susceptibility to C. jejuni infection when administered systemically. These results indicate that MyD88-deficient mice could be a useful model to study C. jejuni colonization and reveal a potential role for Nramp1 in the control of this bacterial pathogen.
Insights
Mice lacking myeloid differentiation factor 88 (MyD88) can be colonized by Campylobacter jejuni, unlike normal mice. This discovery suggests MyD88-deficient mice are a valuable model for studying C. jejuni infection and Nramp1
Area of Science:
- Microbiology
- Immunology
- Infectious Diseases
Background:
- Campylobacter jejuni is a leading cause of global enteric illness.
- Standard adult mice are resistant to C. jejuni infection.
- Myeloid differentiation factor 88 (MyD88) is crucial for Toll-like receptor signaling.
Purpose of the Study:
- To investigate the susceptibility of MyD88-deficient mice to C. jejuni colonization.
- To explore the role of Nramp1 in controlling C. jejuni infection.
Main Methods:
- Colonization experiments with C. jejuni in wild-type and MyD88-deficient mice.
- Infection studies involving Nramp1-deficient mice.
- Analysis of C. jejuni isogenic derivatives with mutations in virulence genes.
Main Results:
- MyD88-deficient mice exhibited stable C. jejuni colonization.
- C. jejuni strains with mutations in known virulence genes failed to colonize MyD88-deficient mice.
- Nramp1 deficiency enhanced susceptibility to systemic C. jejuni infection.
Conclusions:
- MyD88-deficient mice represent a promising model for studying C. jejuni colonization.
- Nramp1 may play a significant role in host defense against C. jejuni.
- Understanding these host-pathogen interactions can inform strategies against enteric illnesses.
