Gastrointestinal Microbiota and Local Inflammation during Oxazolone-induced Dermatitis in BALB/cA Mice.

Lundberg R, Clausen SK, Pang W, Nielsen DS, Möller K, Josefsen KE, Hansen, AK.
Journal   Comparative Medicine
Species  
Analytes Measured   IL-10 , IL-12 Total , IL-2 , IL-4 , IL-5
Matrix Tested   Ear tissue homogenates
Year   2012
Volume   62
Page Numbers   371-380
Application   Cytokines and Chemokines
Abstract
At present, laboratory animals are not standardized with regard to the gastrointestinal microbiota (GM), but differences in this feature may alter various parameters in animal models. We hypothesized that variation in the GM correlated with variation in clinical parameters of a murine oxazolone-induced skin inflammation model of atopic dermatitis. BALB/cA mice were sensitized with oxazolone over a 28-d period and variation in gastrointestinal microbiota in fecal and cecal samples was assessed by PCR-denaturing gradient gel electrophoresis. Clinical parameters included transepidermal water loss, ear thickness, inflammatory factors in ear tissue and plasma, and histopathologic evaluation. The fecal microbiota before induction of skin inflammation strongly correlated with the levels of some proinflammatory cytokines (IFNγ, IL1β, IL12, and TNFα), the antiinflammatory cytokines IL4 and IL10, and the chemokine KC/GRO that were measured in ear samples at study termination. Cecal microbiota at termination correlated with ear thickness and transepidermal water loss. There was no correlation between cytokine responses and ear thickness or transepidermal water loss. In addition, GM changed during the study period in the oxazolone-treated mice, whereas this was not the case for the control mice. The current study shows that the GM of mice influences the development of oxazolone-induced skin inflammation and that the model itself likely induces a pathophysiologic response that alters the composition of the GM.

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Multiplex
V-PLEX Plus Human Biomarker 39-Plex Kit
CRP, Eotaxin, Eotaxin-3, FGF (basic), GM-CSF, ICAM-1, IFN-γ, IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12/IL-23p40, IL-12p70, IL-13, IL-15, IL-16, IL-17A, IP-10, MCP-1, MCP-4, MDC, MIP-1α, MIP-1β, PlGF, SAA, TARC, Tie-2, TNF-α, TNF-β, VCAM-1, VEGF-A, VEGF-C, VEGF-D, VEGFR-1/Flt-1 | Human
Multiplex
V-PLEX Plus Neuroinflammation Panel 1 Human Kit
CRP, Eotaxin, Eotaxin-3, FGF (basic), ICAM-1, IFN-γ, IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12/IL-23p40, IL-13, IL-15, IL-16, IL-17A, IP-10, MCP-1, MCP-4, MDC, MIP-1α, MIP-1β, PlGF, SAA, TARC, Tie-2, TNF-α, TNF-β, VCAM-1, VEGF-A, VEGF-C, VEGF-D, VEGFR-1/Flt-1 | Human
Multiplex
V-PLEX Neuroinflammation Panel 1 Human Kit
CRP, Eotaxin, Eotaxin-3, FGF (basic), ICAM-1, IFN-γ, IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12/IL-23p40, IL-13, IL-15, IL-16, IL-17A, IP-10, MCP-1, MCP-4, MDC, MIP-1α, MIP-1β, PlGF, SAA, TARC, Tie-2, TNF-α, TNF-β, VCAM-1, VEGF-A, VEGF-C, VEGF-D, VEGFR-1/Flt-1 | Human
Multiplex
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