Dataset Information

Sensitivity to oxazolone induced dermatitis is transferable with gut microbiota in mice.

ABSTRACT: Atopic Dermatitis (AD) has been associated with gut microbiota (GM) dysbiosis in humans, indicating a causative role of GM in AD etiology. Furthermore, the GM strongly correlates to essential disease parameters in the well-known oxazolone-induced mouse model of AD. Here, we demonstrate that it is possible to transfer both a high-responding and a low-responding AD phenotype with GM from conventional mice to germ-free mice. The mice inoculated with the high-responding GM had significantly higher clinical score, increased ear thickness, and increased levels of IL-1?, TNF?, IL-4, IL-5, and IL-6 compared to the mice inoculated with the low-responding GM. The inter-individual variation was in general not affected by this increase in effect size. Germ-free mice induced with AD revealed a high disease response as well as high inter-individual variation indicating protective properties of certain microbial taxa in this model. This study underlines that the GM has a strong impact on AD in mouse models, and that the power of studies may be increased by the application of mice inoculated with a specific GM from high responders to increase the effect size.

SUBMITTER: Zachariassen LF

PROVIDER: S-EPMC5349591 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature

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Sensitivity to oxazolone induced dermatitis is transferable with gut microbiota in mice.

Zachariassen Line Fisker LF Krych Lukasz L Engkilde Kåre K Nielsen Dennis Sandris DS Kot Witold W Hansen Camilla Hartmann Friis CH Hansen Axel Kornerup AK

Scientific reports 20170314

Atopic Dermatitis (AD) has been associated with gut microbiota (GM) dysbiosis in humans, indicating a causative role of GM in AD etiology. Furthermore, the GM strongly correlates to essential disease parameters in the well-known oxazolone-induced mouse model of AD. Here, we demonstrate that it is possible to transfer both a high-responding and a low-responding AD phenotype with GM from conventional mice to germ-free mice. The mice inoculated with the high-responding GM had significantly higher c ...[more]

PMID: 28290517

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Project description:There has been a rapid increase in neonates born with a history of prenatal opioid exposure. How prenatal opioid exposure affects pain sensitivity in offspring is of interest, as this may perpetuate the opioid epidemic. While few studies have reported hypersensitivity to thermal pain, potential mechanisms have not been described. This study posits that alterations in the gut microbiome may underly hypersensitivity to pain in prenatally methadone-exposed 3-week-old male offspring, which were generated using a mouse model of prenatal methadone exposure. Fecal samples collected from dams and their offspring were subjected to 16s rRNA sequencing. Thermal and mechanical pain were assessed using the tail flick and Von Frey assays. Transcriptomic changes in whole brain samples of opioid or saline-exposed offspring were investigated using RNA-sequencing, and midbrain sections from these animals were subjected to qPCR profiling of genes related to neuropathic and inflammatory pain pathways. Prenatal methadone exposure increased sensitivity to thermal and mechanical pain and elevated serum levels of IL-17a. Taxonomical analysis revealed that prenatal methadone exposure resulted in significant alterations in fecal gut microbiota composition, including depletion of Lactobacillus, Bifidobacterium, and Lachnospiracea sp and increased relative abundance of Akkermansia, Clostridium sensu stricto 1, and Lachnoclostridium. Supplementation of the probiotic VSL#3 in dams rescued hypersensitivity to thermal and mechanical pain in prenatally methadone-exposed offspring. Similarly, cross-fostering prenatally methadone-exposed offspring to control dams also attenuated hypersensitivity to thermal pain in opioid-exposed offspring. Modulation of the maternal and neonatal gut microbiome with probiotics resulted in transcriptional changes in genes related to neuropathic and immune-related signaling in whole brain and midbrain samples of prenatally methadone-exposed offspring. Together, our work provides compelling evidence of the gut-brain-axis in mediating pain sensitivity in prenatally opioid-exposed offspring.

Dataset Information

Sensitivity to oxazolone induced dermatitis is transferable with gut microbiota in mice.

Publications

Sensitivity to oxazolone induced dermatitis is transferable with gut microbiota in mice.

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