The absence of a microbiota enhances TSLP expression in mice with defective skin barrier but does not affect the severity of their allergic inflammation.

Academic Article

Abstract

  • Evidence is accumulating to suggest that our indigenous microbial communities (microbiota) may have a role in modulating allergic and immune disorders of the skin. To examine the link between the microbiota and atopic dermatitis (AD), we examined a mouse model of defective cutaneous barrier function with an AD-like disease due to loss of Notch signaling. Comparisons of conventionally raised and germ-free (GF) mice revealed a similar degree of allergic skin inflammation, systemic atopy, and airway hypersensitivity. GF mutant animals expressed significantly higher levels of thymic stromal lymphopoietin, a major proinflammatory cytokine released by skin with defective barrier function, resulting in a more severe B-lymphoproliferative disorder that persisted into adulthood. These findings suggest a role for the microbiota in ameliorating stress signals released by keratinocytes in response to perturbation in cutaneous barrier function.
  • Published In

    Keywords

  • Alleles, Animals, Cytokines, Female, Gene Expression Regulation, Genotype, Hypersensitivity, Immunoglobulin E, Immunoglobulin J Recombination Signal Sequence-Binding Protein, Inflammation, Keratinocytes, Male, Mice, Mice, Knockout, Microbiota, Skin
  • Digital Object Identifier (doi)

    Author List

  • Yockey LJ; Demehri S; Turkoz M; Turkoz A; Ahern PP; Jassim O; Manivasagam S; Kearney JF; Gordon JI; Kopan R
  • Start Page

  • 2714
  • End Page

  • 2721
  • Volume

  • 133
  • Issue

  • 12