| First Author | Lee TY | Year | 2014 |
| Journal | J Invest Dermatol | Volume | 134 |
| Issue | 3 | Pages | 704-711 |
| PubMed ID | 24025551 | Mgi Jnum | J:205927 |
| Mgi Id | MGI:5547439 | Doi | 10.1038/jid.2013.389 |
| Citation | Lee TY, et al. (2014) Oral Administration of Poly-gamma-Glutamate Ameliorates Atopic Dermatitis in Nc/Nga Mice by Suppressing Th2-Biased Immune Response and Production of IL-17A. J Invest Dermatol 134(3):704-11 |
| abstractText | Atopic dermatitis (AD) is a chronic inflammatory skin disease that is closely related to dysregulation of the T helper type 1 and 2 (Th1)/Th2 balance. A previous study showed that high molecular mass poly-gamma-glutamate (gamma-PGA) isolated from Bacillus subtilis sp. Chungkookjang induces the production of IL-12 from dendritic cells (DCs). Here, we investigated the effect of gamma-PGA on AD-like skin disease using an Nc/Nga mouse model. In vitro, gamma-PGA activated DCs and induced IL-12 production in mice. In vivo, oral administration of gamma-PGA markedly reduced the AD symptoms, similar to the response seen in the dexamethasone (Dex)-treated group. Treatment with gamma-PGA also decreased the serum levels of IgG1, the skin levels of Th2 cytokines, the extent of skin inflammation, and the accumulation of mast cells. Furthermore, gamma-PGA was effective against established AD, significantly decreasing serum IgE and Th2 cytokines in the inflamed tissue. Interestingly, the production of IL-17A in splenocytes was also suppressed by gamma-PGA, indicating that it inhibits both Th2 and Th17 immune responses. Collectively, these results suggest that oral administration of gamma-PGA could be a therapeutic strategy for treating AD via the modulation of Th2-biased immune responses in an Nc/Nga mouse model. |
