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Quantitative Polymerase Chain Reaction-based Analyses of Murine Intestinal Microbiota After Oral Antibiotic Treatment

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Published on: November 17, 2018

Quantitative dose-response analysis untangles host bottlenecks to enteric infection.

Ian W Campbell^1,2, Karthik Hullahalli^1,2, Jerrold R Turner^3,4

¹Division of Infectious Diseases, Brigham & Women's Hospital, Boston, USA.

Nature Communications

|January 28, 2023

Summary

The host microbiota forms a critical bottleneck, controlling Citrobacter rodentium infection size. This barrier prevents disease by limiting pathogen founding populations, highlighting the microbiota

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Area of Science:

Microbiology
Immunology
Infectious Diseases

Background:

Host defense mechanisms, such as colonization bottlenecks, are crucial for preventing infections by eliminating invading pathogens.
Understanding the factors that influence the establishment and size of pathogen populations is key to comprehending infection dynamics.

Purpose of the Study:

To investigate the role of host-specific factors, particularly the microbiota, in shaping the founding population size of Citrobacter rodentium during infection.
To determine how the dose of inoculum and host conditions affect the severity of colonization bottlenecks.

Main Methods:

Utilized a barcoded population of Citrobacter rodentium to monitor bacterial diversity during colonization in a mouse model.
Manipulated host factors including stomach acid levels, host genotype, and gut microbiota composition.
Quantified the relationship between inoculum dose and the size of the founding pathogen population.

Main Results:

In female mice, the founding pathogen population size scaled with inoculum dose, controlled by a severe but slow-acting bottleneck.
Modest relaxation of the bottleneck occurred with reduced stomach acid or altered host genotype, but the dose-founder relationship persisted.
Disruption of the microbiota eliminated the dose-scaling of the founding population, allowing infection at nearly any dose and indicating the microbiota as the dominant bottleneck.

Conclusions:

The gut microbiota imposes the primary colonization bottleneck, dictating pathogen infectious dose.
Loss of virulence factors, like the locus of enterocyte effacement (LEE), occurs in the pathogen population when microbial competition is absent.
The impact of inoculum dose on the founding pathogen population size is a generalizable metric for defining colonization bottleneck mechanisms.