Kui-Cheng Zheng

Effect of Dietary Vitamin E Supplementation on Murine Nasal Allergy

BACKGROUND Although many studies have reported the effects of dietary vitamin E on the immune response, none so far has assessed its role in nasal allergy. METHODS Female BALB/c mice were randomized into two groups and fed a 20% casein diet (control group, 50 mg vitamin E/kg diet) or this diet supplemented with 535 mg vitamin E/kg diet (vitamin E group, 585 mg vitamin E/kg diet) for 4 weeks. During the fifth week, the mice in each group were divided into two subgroups to form a total of four treatment groups: group A (control), group B [control + toluene diisocyanate (TDI) sensitization], group C (vitamin E supplementation), and group D (vitamin E supplementation + TDI sensitization). Groups B and D were treated with two courses of intranasal application of 5% TDI in ethyl acetate, whereas groups A and C were treated with ethyl acetate alone. A week after second sensitization all groups were provoked by applying 2.5% of TDI in the vehicle and nasal allergic responses were observed for 10 minutes. Splenic lymphoproliferation, splenic cell cytokines, and the total serum IgE were measured. RESULTS Members of group D had lower (P < 0.01) scores of nasal response and sneezed less frequently (P < 0.01) than those of group B. Similarly, splenic lymphoproliferation and production of IL-4 and IL-5 as well as the total serum IgE levels were lower (P < 0.01) in group D than in group B. CONCLUSIONS The results indicate that higher doses of vitamin E supplementation may suppress nasal allergic responses.

Potassium excretion in healthy Japanese women was increased by a dietary intervention utilizing home-parcel delivery of Okinawan vegetables.

Potassium, which is abundant in vegetables, is inversely related to blood pressure. Although the situation has changed somewhat in recent years, the Okinawan diet has generally included a large amount of vegetables, and until recently Okinawans had the lowest rates of mortality due to stroke and coronary heart disease in Japan. Based on the hypothesis that these low mortality rates are partly attributable to increased potassium intake resulting from the high vegetable consumption, this study examined whether increasing the consumption of typical yellow-green Okinawan vegetables increases potassium intake. The purpose of this investigation was to determine whether increased consumption of these vegetables should be one of the dietary modifications recommended in public health promotion programs for Okinawans. The study employed 56 healthy, normotensive, free-living Japanese women aged 18–38 years living in Okinawa. They were randomized to a dietary intervention group (n=27) or a control group (n=29). Members of the dietary intervention group received an average weight of 371.4 g/day of a combination of the following vegetables twice weekly through an express home parcel deliver service for a period of 14 days: Goya (Momordica charantia), green papaya (Carica papaya), Handama (Gynura bicolor), Karashina (Brassica juncea), Njana (Crepidiastrum lanceolatium), Fuchiba (Artemisia vulgaris) and Fudanso (Beta vulgaris); and they consumed an average of 144.9 g/day, resulting in a 20.5% increase in their urinary potassium excretion over the baseline (p=0.045). The members of the control group were asked to avoid these vegetables, and the change in potassium excretion in this group was not significant (p=0.595). Urinary sodium and magnesium excretions, systolic and diastolic blood pressures, folic acid, triglycerides and serum high density lipoprotein cholesterol, low density lipoprotein cholesterol and total cholesterols changed non-significantly in both groups. Also, post-intervention urinary potassium excretion correlated positively with vegetable consumption in both the dietary intervention (p<0.0001) and control (p=0.008) groups and with Okinawan vegetable intake in the dietary intervention group (p=0.0004).

Interleukin-4 and Interleukin-5 Expression in Mice Exposed to 2, 4-Toluene Diisocyanate

lnterleukin‐4 and lnterleukin‐5 Expression in Mice Exposed to 2, 4‐Toluene Diisocyanate: Kui‐Cheng Zheng, et al. Department of Preventive Medicine, Faculty of Medicine, University of the Ryukyus, Okinawa—This study was aimed at investigating the cytokine status and their gene expressions in airways of asthmatic mouse caused by toluene diisocyanate (TDI). After the mice were exposed to TDI vapor for 5 consecutive days, bronchoalveolar lavage (BAL) was carried out and the cells in the BAL fluid were counted. Lung histological test was conducted to analyse the inflammatory status in the airways. Total serum IgE and IL‐4 and IL‐5 concentrations in the BAL fluid were determined with ELISA kits. RT‐PCR was applied to investigate IL‐4 and IL‐5 mRNA from BAL cells. The airway cell count and histological analysis showed that TDI exposure resulted in airway inflammatory responses characterized by marked infiltration of eosinophils in the central and peripheral airways. Total serum IgE was significantly increased in the TDI‐exposed mice. IL‐4 and IL‐5 productions in the BAL fluid were significantly enhanced in the mice exposed to TDI, but in BAL cells IL‐4 and IL‐5 mRNA were slightly enhanced without any significant difference compared to the control mice. These results further support the hypothesis that Th2 cytokines are predominantly produced in TDI‐induced airway hypersensitivity, but our data were not able to indicate the exact source of these cytokines and we could not determine whether the change in cytokines in the airways was controlled by the gene transcription level.

Cytokine Profiles in Airways of Rats Exposed to Toluene Diisocyanate.

Cytokine Profiles in Airways of Rats Exposed to Toluene Diisocyanate: Kui‐Cheng Zheng, et al. Department of Preventive Medicine, School of Medicine, University of the Ryukyus—To investigate the status of cytokines in asthmatic airways induced by toluene diisocyanate (TDI), we established a Wistar rat model for asthma, and did a quantitative determination of cytokine production in asthmatic rats induced by TDI. Rats were sensitized with two courses of intranasal application of 10% TDI with each course for seven consecutive days, and then provoked with 5% TDI, and were followed by observation for airway symptoms. Bronchoalveolar lavage (BAL) was carried out, and total and differential leucocytes from BAL fluid were counted. Lungs were histopathologically examined for the status of inflammation in the airways. The selected cytokines, IL‐2, IL‐4, IL‐6 and IFN‐γ productions, in BAL fluid in vivo and from BAL cells cultured in vitro were quantified with ELISA kits. The results showed that the rats with TDI sensitization exhibited asthmatic symptoms. TDI exposure resulted in an increase in the total number of cells, particularly eosinophils and neutrophils in BAL fluid. Histopathological examination showed a marked infiltration of central and peripheral airways with eosinophils in TDI‐exposed rats. In TDI‐sensitized rats, the productions of IL‐4 and IL‐6 in BAL fluid in vivo were markedly increased compared to that in control rats, but production of IL‐2 and IFN‐ywas similar in the two groups. The cytokines from BAL cells cultured in vitro were released in a similar pattern as in vivo. These findings indicate that IL‐4 and IL‐6 are predominantly secreted in the airways and may play an important role in the pathogenesis of TDI‐induced occupational allergic asthma.

IL-4 and IL-5 Secretions Predominate in the Airways of Wistar Rats Exposed to Toluene Diisocyanate Vapor

Objectives We established a Wistar rat model of asthma caused by toluene diisocyanate (TDI) exposure, and investigated the relationship between TDI exposure concentrations and respiratory hypersensitivity, airway inflammation, and cytokine secretions in animals, to better understand the mechanism of TDI induced occupational asthma. Methods Wistar rats were exposed to two different concentrations of TDI vapor four hours a day for five consecutive days. Bronchoalveolar lavage (BAL) was performed, and differential leucocytes from the BAL fluid were analyzed. Lung histopathological examination was carried out to investigate the inflammatory status in the airways. Production of cytokines interleukin (IL)-4 and IL-5 productions in the BAL fluid in vivo was determined with enzyme-linked immunosorbent assay kits. Results The TDI-exposed rats exhibited greater airway hypersensitivity symptoms than the control rats. The BAL differential cell count and lung histopathological examination demonstrated that inflammation reactions were present in both the central and peripheral airways, characterized with marked infiltration of eosinophils in the TDI-exposed rats. The cytokine assay showed that IL-4 and IL-5 were predominantly produced in the BAL fluid in vivo. Conclusions These findings imply that TDI exposure concentrations may greatly affect the occurrence and extent of inflammatory events and that Th2 type cytokines may play an important role in the immunopathogenesis of TDI-induced occupational respiratory hypersensitivity.