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Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
Dissemination of persistent intestinal bacteria via the mesenteric lymph nodes causes typhoid relapse
Amanda J Griffin1, Lin-Xi Li, Sabrina Voedisch
1Center for Infectious Diseases and Microbiology Translational Research, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, McGuire Translational Research Facility, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
Abstract:
Enteric pathogens can cause relapsing infections in a proportion of treated patients, but greater understanding of this phenomenon is hindered by the lack of appropriate animal models. We report here a robust animal model of relapsing primary typhoid that initiates after apparently successful antibiotic treatment of susceptible mice. Four days of enrofloxacin treatment were sufficient to reduce bacterial loads below detectable levels in all major organs, and mice appeared otherwise healthy. However, any interruption of further antibiotic therapy allowed renewed fecal shedding and renewed bacterial growth in systemic tissues to occur, and mice eventually succumbed to relapsing infection. In vivo imaging of luminescent Salmonella identified the mesenteric lymph nodes (MLNs) as a major reservoir of relapsing infection. A magnetic-bead enrichment strategy isolated MLN-resident CD11b(+) Gr-1(-) monocytes associated with low numbers of persistent Salmonella. However, the removal of MLNs increased the severity of typhoid relapse, demonstrating that this organ serves as a protective filter to restrain the dissemination of bacteria during antibiotic therapy. Together, these data describe a robust animal model of typhoid relapse and identify an important intestinal phagocyte subset involved in protection against the systemic spread of enteric infection.
Insights
A new animal model reveals how typhoid relapses after antibiotic treatment. Mesenteric lymph nodes act as a reservoir, but also protect against infection spread.
Area of Science:
- Microbiology
- Immunology
- Infectious Diseases
Background:
- Relapsing enteric infections pose a clinical challenge.
- Lack of suitable animal models impedes understanding of relapse mechanisms.
Purpose of the Study:
- To develop and characterize a robust animal model for studying relapsing typhoid.
- To identify host factors and reservoirs contributing to typhoid relapse after antibiotic treatment.
Main Methods:
- Established a mouse model of primary typhoid using Salmonella.
- Administered enrofloxacin antibiotic treatment and monitored bacterial loads and clinical outcomes.
- Utilized in vivo imaging to track Salmonella dissemination.
- Employed magnetic-bead enrichment to isolate and analyze immune cells from mesenteric lymph nodes (MLNs).
Main Results:
- Antibiotic treatment reduced bacterial loads but did not prevent relapse upon therapy interruption.
- Mesenteric lymph nodes (MLNs) were identified as a key reservoir for persistent Salmonella.
- A specific monocyte subset (CD11b(+) Gr-1(-)) in MLNs harbored low bacterial numbers.
- MLN removal exacerbated typhoid relapse, indicating a protective role.
Conclusions:
- The developed model effectively replicates relapsing typhoid in mice.
- MLNs serve a dual role in typhoid relapse: as a bacterial reservoir and a protective filter against systemic spread.
- Specific intestinal phagocytes in MLNs are involved in controlling bacterial dissemination during antibiotic therapy.
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