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Immunosuppression of the trimellitic anhydride-induced th2 response by novel nonanatural products mixture in mice.

Bae MJ, Shin HS, Shon DH - Evid Based Complement Alternat Med (2013)

Bottom Line: To characterize the mechanism of this effect, we examined NPM-9 immunosuppression on an OVA-induced Th2 allergic state.NPM-9 also downregulated the polarized Th2 response, whereas it upregulated Th1 response in splenocytes.These data suggest that NPM-9 may be a useful therapeutic agent for allergic inflammatory diseases through its suppression of the Th2-mediated allergic response.

View Article: PubMed Central - PubMed

Affiliation: Korea Food Research Institute, 1201-62 Anyangpangyo-ro, Bundang-gu, Seognam-si, Kyeonggi-do 463-746, Republic of Korea ; Institute for Basic Science, School of Biological Sciences, Seoul National University, 599 Gwanak-ro, Gwanak-gu, Seoul 151-742, Republic of Korea.

ABSTRACT
Many natural dietary products prevent or cure allergic inflammation; however, the ability of mixtures of these natural medicinals to suppress allergic skin inflammation is unknown. We examined the inhibitory effects of nonanatural products mixture (NPM-9), which provides immunoregulatory activation, on Th2-mediated skin allergic inflammation. Oral administration of NPM-9 in mice reduced ear thickness and specific IgE production in trimellitic anhydride- (TMA-)induced contact hypersensitivity (CHS). NPM-9 also suppressed IL-4 and IL-1β production in splenocytes but prevented only TMA-induced IL-1β production in inflamed ears. To characterize the mechanism of this effect, we examined NPM-9 immunosuppression on an OVA-induced Th2 allergic state. Oral administration of NPM-9 inhibited Th2-mediated serum IgE overproduction. NPM-9 also downregulated the polarized Th2 response, whereas it upregulated Th1 response in splenocytes. These data suggest that NPM-9 may be a useful therapeutic agent for allergic inflammatory diseases through its suppression of the Th2-mediated allergic response.

No MeSH data available.


Related in: MedlinePlus

Experimental protocol and ear thickness in TMA-induced CHS mouse model. (a) Experimental protocol. (b) BALB/c mice were divided into naïve, sham (TMA), NPM-9 (250 mg/kg BW), and prednisolone groups (30 mg/kg BW). Ear epidermal thickness was measured by histological analysis (H&E staining). Values are presented as mean ± SD (n = 4 in each group). Data were analyzed by ANOVA followed by Student's t test. *P < 0.05, **P < 0.01, significantly different from the saline value.
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fig2: Experimental protocol and ear thickness in TMA-induced CHS mouse model. (a) Experimental protocol. (b) BALB/c mice were divided into naïve, sham (TMA), NPM-9 (250 mg/kg BW), and prednisolone groups (30 mg/kg BW). Ear epidermal thickness was measured by histological analysis (H&E staining). Values are presented as mean ± SD (n = 4 in each group). Data were analyzed by ANOVA followed by Student's t test. *P < 0.05, **P < 0.01, significantly different from the saline value.

Mentions: TMA induction of CHS was performed as described in [21]. A schematic of the experimental procedure is shown in Figure 2(a). To induce CHS, mice were divided into naïve, sham, NPM-9, and prednisolone groups. Mice were sensitized with 50 μL of 5% TMA (Sigma-Aldrich, St. Louis, MO) in solvent on shaved flank skin on day 0. Challenges with 10 μL of 5% TMA in solvent on the dorsum of both ears were performed on day 5. In the chronic model, animals received challenges on the ears with 10 μL of 2% TMA in solvent on days 6–15. A solvent control group was exposed to acetone and isopropyl myristate (4 : 1, v/v) throughout the duration of the experiment. In the treatment groups, NPM-9 (250 mg/kg body weight (BW)) and prednisolone (30 mg/kg BW), which served as a positive control, were administered orally 1 h before challenge. Each treatment was performed on days 9–15. Body weight and water intake were measured daily. Ear thickness was determined with a custom-built micrometer (Schering AG, Germany). Ears were mechanically homogenized in 2 mL PBS (Sigma-Aldrich, St. Louis, MO), centrifuged at 25,000 g for 30 min at room temperature, and cultured in the presence of 5 μg/mL ConA. Cytokines were measured in the supernatant. Blood samples were obtained from the brachial plexus to estimate the immunoglobulin titer by ELISA 24 h after the final treatment. Spleens were removed and incubated with 5 μg/mL ConA for 72 h. Cytokine production was measured by ELISA.


Immunosuppression of the trimellitic anhydride-induced th2 response by novel nonanatural products mixture in mice.

Bae MJ, Shin HS, Shon DH - Evid Based Complement Alternat Med (2013)

Experimental protocol and ear thickness in TMA-induced CHS mouse model. (a) Experimental protocol. (b) BALB/c mice were divided into naïve, sham (TMA), NPM-9 (250 mg/kg BW), and prednisolone groups (30 mg/kg BW). Ear epidermal thickness was measured by histological analysis (H&E staining). Values are presented as mean ± SD (n = 4 in each group). Data were analyzed by ANOVA followed by Student's t test. *P < 0.05, **P < 0.01, significantly different from the saline value.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3852580&req=5

fig2: Experimental protocol and ear thickness in TMA-induced CHS mouse model. (a) Experimental protocol. (b) BALB/c mice were divided into naïve, sham (TMA), NPM-9 (250 mg/kg BW), and prednisolone groups (30 mg/kg BW). Ear epidermal thickness was measured by histological analysis (H&E staining). Values are presented as mean ± SD (n = 4 in each group). Data were analyzed by ANOVA followed by Student's t test. *P < 0.05, **P < 0.01, significantly different from the saline value.
Mentions: TMA induction of CHS was performed as described in [21]. A schematic of the experimental procedure is shown in Figure 2(a). To induce CHS, mice were divided into naïve, sham, NPM-9, and prednisolone groups. Mice were sensitized with 50 μL of 5% TMA (Sigma-Aldrich, St. Louis, MO) in solvent on shaved flank skin on day 0. Challenges with 10 μL of 5% TMA in solvent on the dorsum of both ears were performed on day 5. In the chronic model, animals received challenges on the ears with 10 μL of 2% TMA in solvent on days 6–15. A solvent control group was exposed to acetone and isopropyl myristate (4 : 1, v/v) throughout the duration of the experiment. In the treatment groups, NPM-9 (250 mg/kg body weight (BW)) and prednisolone (30 mg/kg BW), which served as a positive control, were administered orally 1 h before challenge. Each treatment was performed on days 9–15. Body weight and water intake were measured daily. Ear thickness was determined with a custom-built micrometer (Schering AG, Germany). Ears were mechanically homogenized in 2 mL PBS (Sigma-Aldrich, St. Louis, MO), centrifuged at 25,000 g for 30 min at room temperature, and cultured in the presence of 5 μg/mL ConA. Cytokines were measured in the supernatant. Blood samples were obtained from the brachial plexus to estimate the immunoglobulin titer by ELISA 24 h after the final treatment. Spleens were removed and incubated with 5 μg/mL ConA for 72 h. Cytokine production was measured by ELISA.

Bottom Line: To characterize the mechanism of this effect, we examined NPM-9 immunosuppression on an OVA-induced Th2 allergic state.NPM-9 also downregulated the polarized Th2 response, whereas it upregulated Th1 response in splenocytes.These data suggest that NPM-9 may be a useful therapeutic agent for allergic inflammatory diseases through its suppression of the Th2-mediated allergic response.

View Article: PubMed Central - PubMed

Affiliation: Korea Food Research Institute, 1201-62 Anyangpangyo-ro, Bundang-gu, Seognam-si, Kyeonggi-do 463-746, Republic of Korea ; Institute for Basic Science, School of Biological Sciences, Seoul National University, 599 Gwanak-ro, Gwanak-gu, Seoul 151-742, Republic of Korea.

ABSTRACT
Many natural dietary products prevent or cure allergic inflammation; however, the ability of mixtures of these natural medicinals to suppress allergic skin inflammation is unknown. We examined the inhibitory effects of nonanatural products mixture (NPM-9), which provides immunoregulatory activation, on Th2-mediated skin allergic inflammation. Oral administration of NPM-9 in mice reduced ear thickness and specific IgE production in trimellitic anhydride- (TMA-)induced contact hypersensitivity (CHS). NPM-9 also suppressed IL-4 and IL-1β production in splenocytes but prevented only TMA-induced IL-1β production in inflamed ears. To characterize the mechanism of this effect, we examined NPM-9 immunosuppression on an OVA-induced Th2 allergic state. Oral administration of NPM-9 inhibited Th2-mediated serum IgE overproduction. NPM-9 also downregulated the polarized Th2 response, whereas it upregulated Th1 response in splenocytes. These data suggest that NPM-9 may be a useful therapeutic agent for allergic inflammatory diseases through its suppression of the Th2-mediated allergic response.

No MeSH data available.


Related in: MedlinePlus