• The Korea Journal of Herbology
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• v.27 no.6
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• pp.123-129
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• 2012

Objectives : Allergy has been described as an inflammatory with hypersensitivity resulting from seasonal or perennial responses to specific allergens. The root of Platycodon grandiflorum (Jacq.) A. DC.(Platycodi Radix; Campanulaceae) has been traditionally used to treat chronic diseases such as bronchitis, asthma, pulmonary tuberculosis, inflammation and hyperlipidemia. In this study, we examined the effect of 70% ethanol extract of Platycodi Radix (PR-E) on ovalbumin (OVA)-induced airway inflammation in mice. Methods : Mice were sensitized and challenged by OVA inhalation to induced chronic airway inflammation, and then were intragastrically administered PR-E extract at doses of 50 and 200 mg/kg/day from days 21 to 30 consecutively. The levels of allergic mediators such as histamine, OVA-specific immunoglobulin (Ig) E, and cytokines such as IL-4 and IFN-${\gamma}$ were measured in the sera of mice by ELISA. The histological change of lung tissue was observed by hematoxylin and eosin (H&E) staining. Results : PR-E extract significantly decreased the serum levels of histamine, OVA-specific IgE, and Th2 cytokine, IL-4 compared with those in the OVA-induced group. PE-E extract significantly increased the serum level of Th1 cytokine, IFN-${\gamma}$. Based on lung histopathological studies, inflammatory cell infiltration and mucus hypersecretion were inhibited by PE-E extract administration compared to that in the OVA-induced group. Conclusions : These findings indicate that PE-E extract may be useful as an adjuvant therapy for the treatment of bronchial asthma.

• Tuberculosis and Respiratory Diseases
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• v.47 no.4
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• pp.517-524
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• 1999

Background : Airway inflammation and hyperresponsiveness are recognized as major characteristics of bronchial asthma. Airway inflammation has usually been assessed by invasive methods, e.g. BAL or bronchial biopsy, but recent studies proposed induced sputum as another reliable and non-invasive tool to investigate airway inflammation in asthmatic patients. Thus, the relationship between airway inflammation assessed by induced sputum and airway hyperresponsiveness was investigated in asthmatic patient. Method : Airway responsiveness was determined by the concentration that caused a 20% decrease in $FEV_1$($PC_{20}$) after inhaling incremental concentrations of methacholine. The numbers of inflammatory cells and the concentration of eosinophilic cationic protein(ECP) were assessed in induced sputum obtained by inhalation of hypertonic saline(3%). Result: We analyzed sputum induced in 15 stable asthmatic patients. The differential cell count(%) of macrophages, neutrophils, eosinophils and lymphocytes in induced sputum were $39.1{\pm}27.0%$, $29.6{\pm}21.0%$, $28.8{\pm}18.8%$, $1.3{\pm}3.1%$ respectively. The mean value of baseline FEV1(predicted) and ECP were $76.3{\pm}30.3%$ and $1,101{\pm}833{\mu}g/L$ respectively. The geometric mean value of $PC_{20}$ was 0.56 mg/mL. The relationships between the sputum eosinophil and ECP in induced sputum, and between sputum eosinophil and degree of airway responsiveness($PC_{20}$) were found to be significantly correlated (r=0.81, p<0.05 and r=-0.78, p<0.05, respectively). Sputum neutrophils and $PC_{20}$ were not correlated to each other (r=0.11, p=0.69) and a significant negative correlation was found between ECP and baseline $FEV_1$(predicted)(r=-0.62, p<0.05). Conclusion : The results of this study suggest that an induced sputum via a inhalation of hypertonic saline is useful to determine a patient's status of airway inflammation, and airway inflammation is one of the major causal factors in the development of bronchial hyperresponsiveness in asthmatic patients.

• Tuberculosis and Respiratory Diseases
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• v.73 no.2
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• pp.84-92
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• 2012

Background: Asian dust storms can be transported across eastern Asia. In vitro, Asian dust particle-induced inflammation and enhancement of the allergic reaction have been observed. However, the fibrotic effects of Asian dust particles are not clear. Production of transforming growth factor ${\beta}_1$ (TGF-${\beta}_1$) and fibronectin were investigated in the bronchial epithelial cells after exposure to Asian dust particulate matter (AD-PM10). Methods: During Asian dust storm periods, air samples were collected. The bronchial epithelial cells were exposed to AD-PM10 with and without the antioxidant, N-acetyl-L-cysteine (NAC). Then TGF-${\beta}_1$ and fibronectin were detected by Western blotting. The reactive oxygen species (ROS) was detected by the measurement of dicholorodihydrofluorescin (DCF), using a FACScan, and visualized by a confocal microscopy. Results: The expression of TGF-${\beta}_1$, fibronectin and ROS was high after being exposed to AD-PM10, compared to the control. NAC attenuated both TGF-${\beta}_1$ and fibronectin expression in the AD-PM10-exposed the bronchial epithelial cells. Conclusion: AD-PM10 may have fibrotic potential in the bronchial epithelial cells and the possible mechanism is AD-PM10-induced intracellular ROS.

• Environmental Analysis Health and Toxicology
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• v.25 no.2
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• pp.121-129
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• 2010

This study was carried out to investigate whether asian yellow sand dust (AS) has promoting effects of allergen-related airway inflammation and airway hyperresponsiveness, because the number of patient with allergic asthma and atopy, and with chronic bronchial inflammation and pneumonia have increased steadily in the cities of Korea. The appearance of AS collected was all round and flat, and the diameter was mostly below about 5 ${\mu}m$. When mice were treated with AS suspension by intratracheal instillation combined with ovalalbumin(OVA) sensitization chronically, the level of serum L-lactate dehydrogenase (LDH), IgE and histamine, and respiratory resistance was increased. Intratracheal instillation of AS and OVA also enhanced infiltration of eosinophils in the bronchoalveolar lavage fluid (BALF), IgE and eotaxin expression, and T helper type 2 cell derived cytokines of interleukin (IL)-4, IL-13 and IL-5 as major contributors to allergy and asthma. These results indicate that AS elevates allergen-related airway inflammation and airway hyperresponsiveness in mice and may play an important role in the aggravation of respiratory diseases in Korea.

• Journal of Microbiology
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• v.43 no.1
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• pp.11-16
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• 2005

Matrix metalloproteinase (MMP)-9 plays an important role in the pathogenesis of bronchial asthma. Neovastat, having significant antitumor and antimetastatic properties, is classified as a naturally occurring multifunctional antiangiogenic agent. We evaluated the therapeutic effect of Neovastat on airway inflammation in a mouse model of asthma. BALB/c mice were immunized subcutaneously with ovalbumin (OVA) on days 0, 7, 14, and 21 and challenged with inhaled OVA on days 26, 29, and 31. Neovastat was administrated by gavage (5 mg/kg body weight) three times with 12 h intervals, beginning 30 min before OVA inhalation. On day 32, mice were challenged with inhaled methacholine, and enhanced pause (Penh) was measured as an index of airway hyperresponsiveness. The severity of airway inflammation was determined by differential cell count of bronchoalveolar lavage (BAL) fluid. The MMP-9 concentration in BAL fluid samples was measured by ELISA, and MMP-9 activity was measured by zymography. The untreated asthma group showed an increased inflammatory cell count in BAL fluid and Penh value compared with the normal control group. Mice treated with Neovastat had significantly reduced Penh values and inflammatory cell counts in BAL fluid compared with untreated asthmatic mice. Furthermore, mice treated with Neovastat showed significantly reduced MMP-9 concentrations and activity in BAL fluid. These results demonstrate that Neovastat might have new therapeutic potential for airway asthmatic inflammation.

• Tuberculosis and Respiratory Diseases
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• v.59 no.5
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• pp.530-535
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• 2005

Background and Aims : Cigarette smoking induces an inflammatory response in the airways, which may play a key role in the pathogenesis of chronic obstructive pulmonary disease. Interleukin-6 (IL-6) is one of the cytokines that plays an important role in inducing bronchial inflammation. The aim of this study was to determine if the level of the pro-inflammatory cytokine, Interleukin-6, is increased when the bronchial epithelial cells are exposed to a cigarette smoke extract (CSE) and an extract from stop smoking-aiding cigarettes, and examined the safety of these commercially available stop smoking-aiding cigarettes. Method : Bronchial epithelial cells were exposed to CSE from cigarette and stop smoking-aiding cigarettes for 24 hours. ELISA was used to measure the IL-6 levels in the supernatant from each condition. The IL-6 mRNA levels were measured by Taqman Real time RT-PCR. N-acetyl-L-cysteine(NAC) was added to each condition to determine if NAC can inhibit the release of IL-6 from the bronchial epithelial cells when they are exposed to CSE from cigarette and stop smoking-aiding cigarettes. Result : When bronchial epithelial cells were exposed to a CSE from cigarettes and stop smoking-aiding cigarettes, each type of CSE stimulated IL-6 production from the bronchial epithelial cells. The IL-6 mRNA level in the Bronchial epithelial cells was also elevated and NAC was found to inhibit the release of IL-6 from bronchial epithelial cells when they were exposed to the CSE from cigarettes and stop smoking-aiding cigarettes. Conclusion : Commercially available stop smoking-aiding cigarette can induce bronchial inflammation and can be harmful to smokers. Therefore, the safety of these cigarettes for smoking cessation should be evaluated.

• Clinical and Experimental Pediatrics
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• v.53 no.8
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• pp.795-800
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• 2010

Purpose: B cell-activating factor (BAFF) is a tumor-necrosis factor (TNF) superfamily member best known for its role in the survival and maturation of B cells. BAFF activity is observed in naive cells as well as in effector/memory T cells. We aimed to explore whether BAFF in sputum is expressed at elevated levels in asthmatic airways and associated with eosinophilic inflammation, pulmonary function, and bronchial hyperresponsiveness in children. Methods: One hundred and fifty-four asthmatic children and 98 healthy children were enrolled in the study. Sputum supernatants were collected and sputum BAFF and eosinophil cationic protein (ECP) levels were measured. We performed pulmonary function tests and methacholine challenge tests, while measuring total eosinophil count, total serum IgE, and serum ECP in all subjects. Results: Asthmatic children had significantly higher levels of BAFF in induced sputum [26.50 (10.50-100.27) pg/mL] compared to healthy children [18.32 (7.68-44.63) pg/mL; $P$=0.011]. Sputum BAFF positively correlated with sputum eosinophils (${\gamma}$=0.406, $P$<0.001) and sputum ECP (${\gamma}$=0.789, $P$<0.001). Significant negative correlations were found between sputum BAFF and FEV1 (${\gamma}$=-0.291, $P$<0.001) or post-bronchodilator FEV1 (${\gamma}$=-0.334, $P$<0.001), whereas nonsignificant correlations were found between sputum BAFF and bronchial hyperresponsiveness, serum eosinophil count, and serum ECP. Conclusion: These findings suggest that BAFF may play a role in childhood asthma, and BAFF levels in sputum could be a supportive marker that represents airway inflammation, especially eosinophilic inflammation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.6
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• pp.1649-1653
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• 2006

Allergic diseases are the result of Th2-dominated responses to single or multiple environmental allergens. Th2 cytokines regulate these mechanisms of allergic disease at many levels, including initiation, progression, and persistence. The effect of hwangryun-Hae-Dok-Tang (HRHDT) on tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interleukin-4 (IL-4) stimulated inflammation was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide assay, thymus and activation-regulated chemokine (TARC), eotaxin, regulated on activation normal T cells expressed and secreted (RANTES) immunoassay on the human bronchial epithelial microglial cells. From the present study, the crude extract of Hwangryun-Hae-Dok-tang suppressed the TNF-${\alpha}$ and IL-4 stimulated TARC, eotaxin, and RANTES production in the human bronchial epithelial A549 cells. Based on the present results, Hwangryun-Hae-Dok-tang may be useful in the treatment asthmatic allergy by inhibiting TARC, eotaxin, and RANTES chemokines.

• Journal of Chest Surgery
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• v.20 no.1
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• pp.177-181
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• 1987

For the treatment of bronchial stenosis due to trauma, inflammatory and neoplastic lesion, bronchoplastic procedure in the interest of preservation of lung tissue are relatively new developments in the field of thoracic surgery. We reported on case of bronchoplasty using to pericardial patch for the treatment of bronchial stenosis due to chronic inflammation. The patient was 26 years old female and chief complaint was respiratory difficulty. Bronchogram revealed diffuse stenosis of left main bronchus about 4cm and especially, at just below the carina marked narrowing of lumen and fine serration in the wall. At the time of operation, longitudinal incision was made at left main bronchus about 5cm and reconstructed bronchus using to pericadial patch at membranous compartment of bronchus. The postoperative course was uneventful and post-operative follow up bronchography showed that improvement of bronchoplastic segmented region.

• Tuberculosis and Respiratory Diseases
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• v.57 no.6
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• pp.543-552
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• 2004

Background : Airway remodeling of the asthmatic airway, the result of persistent inflammation in the bronchial wall, is associated with irreversible airway obstruction and the severity of asthma. Previous reports had represented that adminitering CpG-oligodeoxynucleotides (CpG-ODN) before sensitization or challenge by allergens inhibits the development of eosinophilic airway inflammation in a murine model of asthma, but the effects of CpG-ODNs on chronic inflammation and airway remodeling had not been characterized. To investigate the influence of CpG-ODNs on chronic inflammation and remodeling of the airway, we performed studies using a murine model of chronic allergen-induced asthma. Methods : Balb/C mice were sensitized to ovalbumin(OVA) and subsequently exposed to nebulized OVA by means of inhalation twice weekly for 7 weeks. CpG-ODNs($30{\mu}g$) was administered intraperitoneally at sensitization. After final inhalation, mice were evaluated for airway hyperresponsiveness, chronic airway inflammation and remodeling. Results : The mice exposed to chronic and recurrent airway challenge with OVA had persistent airway hyperresponsiveness, chronic inflammation and airway remodeling. Mice treated with CpG-ODNs exhibited decreased bronchial hyperresponsiveness, OVA-specific IgE, chronic inflammation and evidence of airway remodeling, including goblet cell hyperplasia and subepithelial fibrosis. Conclusion : CpG-ODNs was thought to prevent chronic inflammation and remodeling changes in a murine model of chronic asthma.