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The cre-inducer doxycycline lowers cytokine and chemokine transcript levels in the gut of mice

  • Animal Genetics • Short Communication
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Abstract

The antibiotic doxycycline is used as an inducer of recombinase (cre)-based conditional gene knockout in mice, which is a common tool to show the effect of disrupted gene functions only in one period of a research animal’s life. However, other types of such antibiotics have been shown to have a strong impact on the immune system. Here we show that in C57BL/6 mice, the most commonly applied strain for genetic modification, doxycycline treatment lowered transcription of the genes Il1b, Il10, Il18, Tnf, Cxcl1, and Cxcl2 in the ileum, and of the gene Il18 in colon. Cytokines and chemokines encoded by these genes are important in the disease expression in a range of mouse models. Although protein abundances only rarely correlate 100% to transcript levels, and the net result, therefore, may be less dramatic, it seems reasonable to be aware that a broad spectrum antibiotic, such as doxycycline, may impact the transgenic animal in ways unrelated to the activation of the gene deletion.

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Acknowledgements

Helene Farlov and Mette Nelander are kindly thanked for taking care of the mice.

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Authors and Affiliations

Authors

Contributions

AKH and SAM planned the study, SAM did the animal work, SAM and SBM did the gene expression assays, AKH did the statistic assays, and AKH wrote the manuscript, which was corrected and accepted by all authors.

Corresponding author

Correspondence to Axel Kornerup Hansen.

Ethics declarations

Animals were used and housed in accordance with the European Union Directive 2010/63/EU under a license (2012–15–2934-00256 C1) issued by the Danish Ministry of Food and Environment.

Conflict of interest

The authors declare that they have no conflict of interest.

Additional information

Communicated by: Maciej Szydlowski

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Hansen, A.K., Malm, S.A. & Metzdorff, S.B. The cre-inducer doxycycline lowers cytokine and chemokine transcript levels in the gut of mice. J Appl Genetics 58, 535–538 (2017). https://doi.org/10.1007/s13353-017-0401-x

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  • DOI: https://doi.org/10.1007/s13353-017-0401-x

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