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A defined multi-kingdom microbial consortium naturalizes the immune system of laboratory mice

Dirty mice experiments suggest that laboratory mice fail to model certain human immune responses due to their limited microbial exposure. The identity, nature, and number of microbes required to normalize the immune system are unknown. Through systematic screening, we uncovered unexpected cross-kingdom microbial interactions and identified four enteric microbes spanning viruses, fungi, and…

A study of laboratory mice reveals that their immune systems can be effectively "naturalized" through exposure to a specific group of microbes. This discovery arises from experiments demonstrating that conventional mice do not accurately mirror certain human immune responses due to their limited microbial diversity. The precise combination of microbes necessary to achieve this normalization remains unclear.

Through rigorous examination, researchers identified a surprising connection between a group of microbes originating from disparate kingdoms — including viruses, fungi, and protists — that can effectively mimic the immune characteristics of both pet store mice and adult humans. This consortium of four enteric microbes proved capable of altering cancer outcomes, shifting tumorigenesis patterns to align with the anatomical development seen in humans with familial adenomatous polyposis.

Additionally, the study showed that this microbial consortium can reproduce the suboptimal immune responses observed in patients undergoing chimeric antigen receptor (CAR) T cell therapy.

The implications of this research are profound, as they suggest that a mere handful of microbes can significantly influence immune states and disease progression. This discovery opens up new avenues for improving the relevance of laboratory mouse models in understanding and treating human immune-related diseases.

Written by urgent.news from bioRxiv's reporting — not their text. Machine-written — may contain errors; check the original before relying on it.

Read the original at biorxiv.org →

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