• The Journal of Internal Korean Medicine
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• v.25 no.3
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• pp.427-439
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• 2004

It has been reported that Bopheyangyoungjeon(BYJ) has an effect on deficiency asthma(喘虛) clinically. The aim of this study was to determine an appropriate dosage of BYJ to treat asthma. In order to study the effects of orally administered BYJ on allergic asthma, mice were pretreated with three oral doses of the herbal solution of BYJ before antigen sensitization. 2 days later Mice were actively sensitized with a subcutaneous injection of ovalbumin and 13 day later ovalbumin aerosols were used to provoke asthmatic reaction. Serum level of IgE, IL-4, WBC, RBC, HGB, cell numbers in bronchoalveolar lavage fluid(BALF), and in vitro isometric contractile responses of the isolated tracheal smooth muscle(TSM) to acetylcholine(ACh, 0.1-1000uM), KCl were measured. The results were as follows ; 1. Contractile responses of TSM to ACh significantly increased in C group at Ach 0.3, 1, 3, 10, 30, 100, 300, 1000uM(P<0.05, P<0.01) and increased in D at 0.1, 0.3, 3, 30, 30, 100, 300, 1000uM. 2. The sensitivity of TSM to Ach increased more in A, B group, but it was not significant. 3. The maximal contractile response of TSM to ACh decreased more significantly in C group(P<0.01) and D group(P<0.05) the control group. 4. The maximal contractile response of TSM to KCI decreased more significantly in B group and C group(P<0.001) than in the control group. 5. The counts of lymphocytes in BALF decreased more significantly in B group and D group(P<0.05) than in the control group. 6. The counts of macrophages in BALF decreased more significantly in B group, C(P<0.05) than in the control group. 8. Serum IgE level increased more significantly in B group and C group(P<0.05) than the control group. 9. The counts of WBC, RBC, HGB in blood increased more significantly in A group than the control group. The above results support a role for BYJ orally administered in treatment of deficiency allergic Asthma.

• Tuberculosis and Respiratory Diseases
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• v.46 no.2
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• pp.175-184
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• 1999

Background: Bronchial asthma is characterized by chronic eosinophilic inflammatory airway disease associated with bronchial hyperresponsiveness and reversible airway obstruction. Bronchial inflammation in asthma may depend in part on the activation of T helper lymphocytes that elaborate proinflammatory cytokines. T helper (Th) lymphocytes can be divided into two categories; Th1 lymphocytes, which secrete IL-2, IL-12 and IFN-$\gamma$, and Th2 lymphocytes, which secrete IL-4, IL-5, IL-6 and IL-10. Th2 lymphocytes appear to induce allergic responses, whereas Th1 lymphocytes induce delayed-type hypersensitivity response. Some infections, such as tuberculosis, cultivate a Th1 immunological environment and inhibit Th2 lymphocytes function. The presence of such infections might inhibit Th2 immune responses and thus protect development of atopic diseases. Method: 15 patients with allergic bronchial asthma, 10 patients with intrinsic bronchial asthma, and 10 healthy volunteers were studied. The serum concentrations of IFN-$\gamma$, IL-12, IL-4, IL-5, and IL-10 were measured by ELISA method and tuberculin skin test was estimated in different groups. Results: The positive response rates of tuberculin test were 46.7% in patients with allergic asthma, 100% in patients with intrinsic asthma and 60% in normal controls. The positive response rates were significantly lower in patients with allergic asthma than those of in patients with intrinsic asthma (p<0.05). Degree of responses to tuberculin test were $12.0{\pm}9.6mm$ in patients with allergic asthma, $18.4{\pm}4.5mm$ in patients with intrinsic asthma and $10.9{\pm}8.8mm$ in normal controls. The degree of responses were significantly reduced in patients with allergic asthma than those of patients with intrinsic asthma (p<0.05). The serum levels of IL-5 in patients with allergic asthma were significantly higher than in patients with intrinsic asthma and normal controls (p<0.05), although it was insignificant. the serum levels of IL-4 and IL-10 in patients with allergic asthma were higher than that of intrinsic asthma and normal controls. The serum levels of IL-12 and IFN-$\gamma$ in patients with allergic asthma and intrinsic asthma were significantly lower than those in normal controls(p<0.05). The serum levels of total immunoglobulin E (IgE) and peripheral blood eosinophile counts in patients with allergic asthma were significantly higher than those in normal controls. Peripheral blood esinophil counts had a significant correlation with the serum levels of total IgE, IL-5 and IL-10 in patients with allergic asthma (p<0.05). Conclusion: These results have showed that Th1 lymphocyte functions were lowered and Th2 lymphocyte functions were elevated in patients with allergic asthma than those in normal controls. Suppression of Th1 lymphocyte functions by activation of Th2 lymphocyte might be one of the important aspects of pathogenesis in allergic bronchial asthma.

• Microbiology and Biotechnology Letters
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• v.38 no.1
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• pp.93-104
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• 2010

In this study, we investigated the effects of frankincense essential oil (BSEO) on the immune cell change in the lung, BALF and PBMC using a mouse model of asthma. BALB/c mice after intraperitoneal OVA sensitization (day 1) were challenged intratracheally with OVA on day 14. Then, the asthma was induced by repeated OVA inhalation challenged. The asthma induced mice group inhaled 0.3% BSEO for 30 minutes per trial, three times a week, for 8 weeks using the nebulizer. After 12 weeks from the experiment, the mice was killed and the lung, bronchoalveolar lavage fluid (BALF) and peripheral blood mononuclear cell (PBMC) were obtained. Next, the change of immune cells inside the separated tissues was observed to identity the effects of BSEO on the allergic asthma mice. In conclusion, the hypersensitive reaction of airway to the bronchoconstrictor in the allergic asthma induced mice was effectively suppressed in Frankincense group, in Bermagot, Eucalyptus, Chamomile, Marjoram and Frankincense groups, the natural aromatic essential oil groups. Furthermore, it was also confirmed that the weight of lung, total number of alveolus cells and the number of BALF, MNL and DLN increased after inducing allergic asthma were reduced. BSEO suppressed the percentage of $CD3e^+/CD19^-$, $B220^+/CD23^+$ and $CD11b^+/Gr-1^+$ cells in the lung tissue of allergic asthma mice. Moreover, BSEO also reduced the percentage of $CD4^+/CD8^-$, $B220^+/CD23^+$ and $CD3^+/CCR3^+$ cells in BALF. In addition, the percentage of $CD3e^+/CD19^-$, $CD3^+/CD69^+$ and $B220^+/CD23^+$ cells in PBMC was reduced. The results of this study indicate that BSEO would be effective to treat allergic asthma by the immune control suppressing the activity of immune cells in each tissue.

• BMB Reports
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• v.45 no.5
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• pp.311-316
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• 2012

Sulforaphane (1-isothiocyanato-4-(methylsulfinyl)-butane), belonging to a family of natural compounds that are abundant in broccoli, has received significant therapeutic interest in recent years. However, the molecular basis of its effects remains to be elucidated. In this study, we attempt to determine whether sulforaphane regulates the inflammatory response in an ovalbumin (OVA)-induced murine asthma model. Mice were sensitized with OVA, treated with sulforaphane, and then challenged with OVA. Sulforaphane administration significantly alleviated the OVA-induced airway hyperresponsiveness to inhaled methacholine. Additionally, sulforaphane suppressed the increase in the levels of SOCS-3 and GATA-3 and IL-4 expression in the OVA-challenged mice. Collectively, our results demonstrate that sulforaphane regulates Th2 immune responses. This sutdy provides novel insights into the regulatory role of sulforaphane in allergen-induced Th2 inflammation and airway responses, which indicates its therapeutic potential for asthma and other allergic diseases.

• Journal of Life Science
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• v.22 no.3
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• pp.298-305
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• 2012

The general term flavonoids is often used to categorize a family of natural compounds that are highly abundant in all higher plants, and which in recent years have attracted scientific interest as therapeutics. Lutein is a xanthophyll and one of 600 known naturally occurring carotenoids. It is found in green vegetables such as spinach and kale, and has been demonstrated to exert anti-inflammatory activities. However, its anti-allergic effect in the Th1/Th2 immune response is poorly understood. In this study, we attempt to determine whether lutein regulates inflammatory mediators in an ovalbumin (OVA)-induced murine asthma model. To address this, mice were sensitized and challenged with OVA, and then treated with lutein before the last OVA challenge. Administration of lutein significantly suppressed the OVA-induced airway hyper-responsiveness. It also resulted in a significant alleviation of the infiltration of inflammatory cells into the bronchoalveolar lavage. Additionally, lutein attenuated the increased expression of Th2 responses in OVA-challenged mice. These results demonstrate that lutein is a potent inhibitor that reduces Th2 immune responses. Furthermore, they show that the immunopharmacological function is mediated by a pathway that involves and is regulated by Th2 immune response.

• Journal of Microbiology and Biotechnology
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• v.31 no.8
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• pp.1109-1114
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• 2021

Chlamydia pneumoniae is a type of pathogenic gram-negative bacteria that causes various respiratory tract infections including asthma. Chlamydia species infect humans and cause respiratory infection by rupturing the lining of the respiratory which includes the throat, lungs and windpipe. Meanwhile, the function of interleukin-4 (IL-4) in Ch. pneumoniae respiratory infection and its association with the development of airway hyperresponsiveness (AHR) in adulthood and causing allergic airway disease (AAD) are not understood properly. We therefore investigated the role of IL-4 in respiratory infection and allergy caused by early life Chlamydia infection. In this study, Ch. pneumonia strain was propagated and cultured in HEp-2 cells according to standard protocol and infant C57BL/6 mice around 3-4 weeks old were infected to study the role of IL-4 in respiratory infection and allergy caused by early life Chlamydia infection. We observed that IL-4 is linked with Chlamydia respiratory infection and its absence lowers respiratory infection. IL-4R α2 is also responsible for controlling the IL-4 signaling pathway and averts the progression of infection and inflammation. Furthermore, the IL-4 signaling pathway also influences infection-induced AHR and aids in increasing AAD severity. STAT6 also promotes respiratory infection caused by Ch. pneumoniae and further enhanced its downstream process. Our study concluded that IL-4 is a potential target for preventing infection-induced AHR and severe asthma.

• Journal of Environmental Health Sciences
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• v.29 no.3
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• pp.35-42
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• 2003

Nitric Oxide(NO) is produced in many organs of the body, including the lung and airways, and it is detectable in the exhaled air. The measurement of exhaled NO(eNO) provides a simple non-invasive means for measuring airway inflammation, such as asthma. We measured eNO among adult male workers to examine the distribution of eNO in healthy people and to find factors affecting eNO. We measured eNO in a sample of 921 adult workers who also performed lung function test and skin prick test. Exhaled NO was measured in a sitting posture without using a nose clip and NO free gas. NO was measured at three expiratory rates(l8; 42; 71 $m\ell$/sec) and the flow rate of 71 $m\ell$/sec was used in analysis. The average eNO concentration was 5.29 $\pm$ 2.98 ppb. The level increased with age but not significantly(P=0.0529). Exhaled NO showed positive relations to the height(P=0.0001), pollen 1 (P=0.0124), asthma history(P=0.0212), allergic rhinitis symptom(P=0.0302). Exhaled NO Concentration of smokers( 4.62 ppb) was significantly lower than that of nonsmokers(5.99 ppb; P<0.0001).

• Tuberculosis and Respiratory Diseases
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• v.48 no.2
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• pp.191-202
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• 2000

Background: Bronchial asthma is characterized by airway hyperresponsiveness(BHR) and inflammation. The cyclooxygenase(COX) is believed to be one of the important enzymes in these inflammatory reactions. Recently, the COX was divided into two isoforms, COX1 and COX2. COX2 is induced by lipopolysaccharide and some cytokines at the inflammation site. Prostaglandin E2(PGE2), produced from COX2, may affect airway inflammation. The purpose of this study is to evaluate the effect of COX2 inhibitor on COX2 expression, plasma PGE2, airway resistance and histologic finding in an animal asthma model. Methods : Sprague-Dawley rats were divided into 3 groups. The normal control group did not receive any treatment, but the asthma control group was sensitized by ovalbumin but not treated with the COX2 inhibitor(nimesulide, Mesulid$^{(R)}$). The treatment group was sensitized and treated with nimesulide. Specific airway resistance(sRaw) before and after nimesulide ingestion was investigated. The PGE2 level in the plasma was examined and COX2 immunogold-silver stain on lung tissue was performed. Results: sRaw and eosionophilic infiltration on airway, which increased in the asthma control group, was compared to normal control(p=0.014). However, there was no difference in eosinophilic infiltration between asthma control and treatment groups(p=0.408) and no difference in COX2 expression on bronchiolar epithelium among the three groups. Plasma PGE2 levels were not statically different among the three groups. Conclusion: The role of COX2 in the allergen-induced BHR was not significant The effect of nimesulide was not observed on BHR, COX2 expression, and plasma PGE2 level. Therefore, COX2 may not be a major substance of allergic asthma.

• Clinical and Experimental Pediatrics
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• v.49 no.9
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• pp.977-982
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• 2006

Purpose : There has been an increasing amount of literature concerning the association between Mycoplasma pneumoniae and asthma pathogenesis. Interleukin(IL)-6 stimulates the differentiation of monocytes, and can promote Th2 differentiation and simultaneously inhibit Th1 polarization. IL-8 is a potent chemoattractant and, it has been suggested, has a role in asthma pathogenesis. Nitric oxide (NO) synthesized by airway epithelium may be important in the regulation of airway inflammation and reactivity. Vascular endothelial growth factor(VEGF) has been reported to be a mediator of airway remodeling in asthma. We investigated the effects of M. pneumoniae on IL-6, IL-8, NO and VEGF production in human respiratory epithelial cells. Methods : A549 cells were cultured and inoculated with M. pneumoniae at a dose of 20 cfu/cell. After infection, the presence of M. pneumoniae in epithelial cell cultures was monitored by immunofluorescence and confirmed by polymerase chain reaction(PCR) detection. IL-6, IL-8 and VEGF were determined by an enzyme-linked immunosorbent assay and reverse transcriptase-polymerase chain reaction. NO was measured using the standard Griess reaction. Results : In A549 cells, M. pneumoniaeinduced IL-6, IL-8, NO and VEGF release in time-dependent manners. It also induced mRNA expression of IL-6, IL-8 and VEGF in similar manners. Conclusion : These observations suggest that M. pneumoniae might have a role in the pathogenesis of the allergic inflammation of bronchial asthma.

• Journal of Pharmacopuncture
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• v.19 no.4
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• pp.303-311
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• 2016

Objectives: Allergic asthma generally presents with symptoms of wheezing, coughing, breathlessness, and airway inflammation. Seonpyejeongcheon-tang (SJT) consists of 12 herbs. It originated from Jeong-cheon-tang (JT), also known as Ding-chuan-tang, composed of 7 herbs, in She-sheng-zhong-miao-fang. This study aimed to evaluate the effects of local delivery of SJT via inhalable microparticles in an asthma mouse model. Methods: Microparticles containing SJT were produced by spray-drying with leucine as an excipient. SJT microparticles were evaluated with respect to their aerodynamic properties, in vitro cytotoxicity, in vivo toxicity, and therapeutic effects on ovalbumin (OVA)-induced asthma in comparison with orally-administered SJT. Results: SJT microparticles provided desirable aerodynamic properties (fine particle fraction of $48.9%{\pm}6.4%$ and mass median aerodynamic diameter of $3.7{\pm}0.3{\mu}m$). SJT microparticles did not show any cytotoxicity against RAW 264.7 macrophages at concentrations of 0.01 - 3 mg/mL. Inhaled SJT microparticles decreased the levels of IL-4, IL-5, IL-13, IL-17A, eotaxin and OVA-IgE in bronchoalveolar lavage fluid (BALF) in mice with OVA-induced asthma. These effects were verified by histological evaluation of the levels of infiltration of inflammatory cells and collagen, destructions of alveoli and bronchioles, and hyperplasia of goblet cells in lung tissues. The effects of SJT microparticles in the asthma model were equivalent to those of orally-administered SJT extract. Conclusion: This study suggests that SJT is a promising agent for inhalation therapy for patients with asthma.