Bibliographic Details
| Title: |
Oral Probiotic Control Skin Inflammation by Acting on Both Effector and Regulatory T Cells. |
| Authors: |
Hacini-Rachinel, Feriel1,2,3, Gheit, Hanane1,2,3, Le Luduec, Jean-Benoit1,2,3, Dif, Fariel4, Nancey, Stéphane1,2,3,5, Kaiserlian, Dominique1,2,3 dominique.kaiserlian@inserm.fr |
| Source: |
PLoS ONE. 2009, Vol. 4 Issue 3, p1-9. 9p. 2 Diagrams, 5 Graphs. |
| Subject Terms: |
*SKIN inflammation, *T cells, *PROBIOTICS, *ALLERGIES, *PROTEINS, *CONTACT dermatitis |
| Abstract: |
Probiotics are believed to alleviate allergic and inflammatory skin disorders, but their impact on pathogenic effector T cells remains poorly documented. Here we show that oral treatment with the probiotic bacteria L. casei (DN-114 001) alone alleviates antigen-specific skin inflammation mediated by either protein-specific CD4+ T cells or hapten-specific CD8+ T cells. In the model of CD8+ T cell-mediated skin inflammation, which reproduces allergic contact dermatitis in human, inhibition of skin inflammation by L. casei is not due to impaired priming of hapten-specific IFNγ-producing cytolytic CD8+ effector T cells. Alternatively, L. casei treatment reduces the recruitment of CD8+ effector T cells into the skin during the elicitation (i.e. symptomatic) phase of CHS. Inhibition of skin inflammation by L. casei requires MHC class II-restricted CD4+ T cells but not CD1d-restricted NK-T cells. L casei treatment enhanced the frequency of FoxP3+ Treg in the skin and increased the production of IL-10 by CD4+CD25+ regulatory T cells in skin draining lymph nodes of hapten-sensitized mice. These data demonstrate that orally administered L. casei (DN-114 001) efficiently alleviate T cell-mediated skin inflammation without causing immune suppression, via mechanisms that include control of CD8+ effector T cells and involve regulatory CD4+ T cells. L. casei (DN-114 001) may thus represent a probiotic of potential interest for immunomodulation of T cell-mediated allergic skin diseases in human. [ABSTRACT FROM AUTHOR] |
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| Database: |
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