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Summary
Animal models are an important tool in investigating molecular mechanisms of disease pathogenesis and in developing therapeutic approaches for human disease. In many instances though, success in preclinical experiments cannot be translated into the human setting (1). One potential explanation for this discrepancy between animal model and human experimental outcomes may involve the microbiota, a large ecosystem of bacteria, fungi, protozoa, and viruses that colonize mucosal surfaces in the human body, particularly the gastrointestinal tract (2). Differences in microbiota diversity, resilience, and presence of pathogens between laboratory animals and other “wild” mammals may lead to a limited reproducibility of animal experimentation when attempted in different localities or when used as models of human disease (3). On page 461 of this issue, Rosshart et al. (4) generate a more physiologically relevant preclinical mouse model by combining the diversity of the microbiota found in wild mice with the genetic uniformity of laboratory animals.
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