Open AccessJapanese traditional medicine, Senn-kinn-naidaku-sann up-regulates Toll-like receptor 4 and reduces murine allergic rhinitis
Author(s) -
I. Morikura,
A. Murata,
N. Aoi,
Y. Shimizu,
T. Fuchiwaki,
E. Prokopakis,
H. Kawauchi
Publication year - 2014
Publication title -
rhinology (amsterdam. online)/rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.275
H-Index - 57
eISSN - 1996-8604
pISSN - 0300-0729
DOI - 10.4193/rhino11.269
Subject(s) - medicine , mucous membrane of nose , tlr4 , spleen , immunology , receptor , sensitization , toll like receptor , cytokine , splenocyte , immunoglobulin e , nasal administration , antibody , immune system , innate immune system
Objective: To determine the mechanisms by which a traditional herbal medicine, Senkinnaidakusan (SKNS), controls Th2 responses, we examined the production of IL-12 by murine macrophages treated with SKNS. Results: Treatment with SKNS significantly increased TLR4 mRNA in macrophages. Furthermore, pre-treatment with SKNS enhanced the production of IL-12 by macrophages stimulated with LPS. When SKNS was orally administered to C3H/HeN mice at the induction phase after OVA sensitization, the serum levels of OVA-specific immunoglobulin (Ig)E and IgG1 decreased, Interleukin (IL)-4 production by spleen T cells in response to OVA was significantly suppressed, while interferon (IFN)-gamma production was increased. After nasal challenge of OVA, eosinophilic infiltration in the nasal mucosa and the number of sneezes were significantly inhibited in SKNS-treated mice compared with control mice. Besides, expression of IL-5 in the nasal mucosa was also inhibited. Using another strain of mice, C3H/HeJ (TLR4 negative), there was no difference in OVA-specific Igs or splenic cytokine production between the SKNS treatment and non-treatment groups. The eosinophilic infiltration in the nasal mucosa, the number of sneezes and IL-5 expression in the nasal mucosa were also not effected even after SKNS treatment. Conclusion: These results suggest that oral administration of SKNS inhibits Th2 responses by enhancement of IL-12 release from macrophages via up-regulation of TLR4 expression.