Yoon, Ho Joo;Kim, Mi Ok;Sohn, Jang Won;Kim, Jung Mogg;Shin, Dong Ho;Park, Sung Soo
Tuberculosis and Respiratory Diseases
/
v.54
no.1
/
pp.104-113
/
2003
Background : Rhinovirus(RV) infections frequently trigger dyspnea and paroxysmal cough in adult patients with asthma and are the most prevalent cause of the common cold. However, the mechanisms of a RV-induced airway inflammation is unclear. Since the RV does not directly destroy the airway epithelium, it is presumed that the immune response to the RV contributes to the pathogenesis of the respiratory symptoms. In order to test this hypothesis, this study characterized the time-sequenced alterations in interleukin(IL)-8 elaboration from the human bronchial epithelial cells and evaluated the role of NF(nuclear factor)-${\kappa}B$ in the RV-induced IL-8 production by pretreating the inhibitors of NF-${\kappa}B$ activation. Methods : The ability of RV-infected human bronchial epithelial cells and BEAS-2B cells to produce the IL-8 was compared with the controls. This study infected BEAS-2B cells with the RV14 obtained from the American Type Culture Collection. The supernatants were harvested from the RV infected BEAS-2B cells and the controls at 2hr, 4hr, 6hr, 12hr, 24hr, 48hr from the inoculation time. This study measured the IL-8 concentration using the ELISA kits. In order to elucidate the role of NF-${\kappa}B$ in the RV-induced IL-8 production, the effect of the NF-${\kappa}B$ inhibitors was evaluated on RV-induced IL-8 production. Results: The BEAS-2B cells produced small amounts of IL-8 that accumulated slowly with time in the culture. The RV was a potent stimulator of the IL-8 proteins production by BEAS-2B human bronchial epithelial cells. Antioxidants, N-acetyl-L-cysteine(NAC),\ and pyrrolidine dithiocarbamate(PDTC), blocked the IL-8 elaboration by the RV-infected BEAS-2B cells, which was dose-dependent, but N-Tosyl-L-phenylalanine chloromethyl ketone(TPCK) did not. Conclusion: Some antioxidants inhibited the RV-induced IL-8 production by blocking the NF-${\kappa}B$, which may have a therapeutic potential in asthma.
Background : The recognition of bronchial asthma as an inflammatory disease led to the search for soluble markers that would be useful in assessing airway inflammation. Interleukin-6 (IL-6) is a representative proinflammatory cytokine that has been shown to be connected with various inflammatory diseases. IL-6 acts via specific receptors that consist of the IL-6 binding glycoprotein gp80 and the signal transducer gp130. In the search for markers of airway inflammation, delete the role of soluble interleukin-6 receptor (sIL-6R) and IL-6 in acute asthma were investigated. Methods : Serum levels of sIL-6R and IL-6 were measured in 78 acute asthmatics, in 15 patients with asymptomatic asthma and in 10 healthy control subjects by a specific ELISA using a murine antihuman IL-6R, IL-6 mAb ($Quantikine^{(R)}sIL$-6R, IL-6). Results : Serum levels of IL-6 in acute asthmatics significantly exceeded those of control subjects. The levels of sIL-6R in acute asthmatics were also significantly increased compared to those of control subjects. The serum concentrations of IL-6 obtained in acute asthmatics were elevated compared with those in asymptomatic asthmatics. However, association between eosinophilic count/IgE and IL-6/sIL-6R in acute asthma could not be found. Conclusion : Our results suggest that IL-6 may be involved in the pathogenesis of acute asthma, and serum levels of IL-6 and sIL-6R may reflect the severity of airway inflammation.
Background : It has been well known that bronchia1 asthma is a chronic airway inflammatory disorder. Recently, sputum induced with hypertonic saline was introduced as a simple and useful nonivasive medium to investigate airway inflammation and symptom severity in patients with asthma. We examined the eosinophil, eosinophil cationic protein (ECP), interleukin(IL)-3, IL-5, granulocyte-macrophage colony-stimulating facta (GM-CSF), and nitric oxide (NO) derivatives in induced sputum from patients with bronchia1 asthma in order to determine the role of NO and various inflammatory cytokines as a useful markers of airway inflammation or changes in pulmonary function tests and symptoms. Methods : A total 30 patients with bronchia1 asthma received oral prednisolone 30 mg daily for 2 weeks. Forced expiratory volume in one second ($FEV_1$), total blood eosinophil count and induced sputum eosinophil count, ECP, IL-3, IL-5, GM-CSF, and NO derivatives were determined before and after the administration of prednisolone. Results : Of the 30 patients, 13 (43.3%) were male and 17 (56.7%) were female. The mean age of patients was 41.8 years (range 19-64 years). Two patients could not produce sputum at the second study and 3 could not be followed up after their first visit. Two weeks after the prednisolone administration, there was a significant increase in $FEV_1$ (% of predicted value) from 78.1$\pm$20.6 % to 90.3$\pm$ 18.3 % (P<0.001). The eosinophil percentages in induced sputum were significantly decreased after treatment with prednisolone, with values of 56.1$\pm$27.2 % versus 29.6$\pm$21.3 % (P<0.001), and ECP were $134.5\pm68.1\;{\mu}g/L$ versus $41.5\pm42.4\;{\mu}g/L$ (P<0.001) respectively. After the prednisolone treatments, the eotaxin concentration also showed a decreasing tendency from 26.7$\pm$12.8 pg/ml to 21.7$\pm$8.7 pg/ml. There was a decreasing tendency but no significant differences in total blood eosinophil count (425.7$\pm$265.9 vs 287.7$\pm$294.7) and in the concentration of NO derivatives ($70.4\pm44.6{\mu}mol/L$ vs $91.5\pm48.3\;{\mu}mol/L$) after the prednisolone treatments. IL-3, IL-5, GM-CSF were undetectable in the sputum of most subjects either before the prednisolone treatments or after the treatments. Before the prednisolone treatments, a significant inverse correlation was observed between FEV1 and sputum ECP (r=-D.364, P<0.05) and there was a significant correlation between sputum eosinophils and eotaxin (r=0.369, P<0.05) Conclusion : The eotaxin and ECP concentration in induced sputum may be used as markers of airway inflammation after treatments in bronchia1 asthma. In addition, the measurement of sputum eosinophil percent ages is believed to be a simple method displaying the degree of airway inflammation and airway obstruction before and after the prednisolone treatment in bronchia1 asthma. However, unlike exhaled NO, the examination of NO derivatives with Griess reaction in induced sputum is considered an ineffective marker of changing airway inflammation and obstructing symptoms.
Purpose : We hypothesized that the persisting bronchial hyperresponsiveness (BHR) of adolescents with asthma remission may be controlled mainly by genetic factors, and the BHR of symptomatic asthma by airway inflammation. ${\beta}_2$-adrenoceptor gene is considered to be a candidate gene in the development of BHR. Thus, ${\beta}_2$-adrenoceptor gene polymorphism may be associated with the BHR of adolescents with asthma remission, but not with the BHR of symptomatic asthma. To evaluate this hypothesis, ${\beta}_2$-adrenoceptor gene polymorphism at 2 sites (Arg16-Gly, Gln27-Glu) were examined. Methods : Two hundred two adolescents with BHR ($PC_{20}<18\;mg/mL$) and long term remission (neither asthma-related symptoms nor medication during the previous 2 years) of their asthma (remission group), 182 adolescents with symptomatic asthma (symptomatic group), and 200 healthy adolescents (control group) were studied. Asthma phenotypes were determined using methacholine bronchial provocation test and skin prick test. Genotypes of ${\beta}_2$-adrenoceptor polymorphism were evaluated by PCR-based methods. Results : Gly/Gly allele and Gly16-Gln27 haplotype were more prevalent in the remission group than in the control group (P=0.01, P=0.02), although there was no difference between the symptomatic group and the control group. In the remission group, there was significant difference in geometric mean of $PC_{20}$ among the 3 groups subdivided by the number of Gly16-Gln27 haplotype, showing that the Gly16-Gln27 haplotype was positively associated with BHR. However, no association was found between Gly16-Gln27 haplotype and BHR in the symptomatic group. Conclusion : This study demonstrates that ${\beta}_2$-adrenoceptor polymorphism at amino acid 16 and 27 was associated with BHR persisting in adolescents with asthma remission.
Lee, Sun Hee;Kim, Do Kyun;Choi, Sun Hee;Koh, Young Yull
Clinical and Experimental Pediatrics
/
v.49
no.11
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pp.1216-1222
/
2006
Purpose : Though atopic and nonatopic asthma have different clinical manifestations, bronchial hyperresponsiveness (BHR) and airway inflammations are common characteristics of them. We investigated BHR to both methacholine and adenosine 5'-monophosphate (AMP), and their relationships with blood eosinophil markers in nonatopic asthma as well as atopic asthma. Methods : We studied 116 children (82 atopics; 34 nonatopics) with mild to moderate asthma. Methacholine and AMP challenge tests were performed and bronchial responsiveness was expressed as $PC_{20}$ (provocative concentration causing a 20 percent fall in $FEV_1$); blood eosinopil counts (ETCs) and serum eosinophil cationic protein (ECP) levels were gauged. Results : In atopics, 95.1 percent and 90.2 percent showed hyperreactivity to methacholine ($PC_{20}$<16 mg/mL) and AMP ($PC_{20}$<200 mg/mL), respectively. Meanwhile, in nonatopics, 94.1 percent and 52.9 percent displayed hyperreactivity to methacholine and AMP, respectively. The geometric mean of AMP $PC_{20}$ was lower in atopics (31.6 mg/mL) than in nonatopics (125.9 mg/mL); that of methacholine $PC_{20}$ was similar in the two groups. AMP $PC_{20}$ correlated with blood ETCs in both atopics(r=-0.30, P<0.01) and nonatopics (r=-0.57, P<0.01), and correlated with serum ECP levels (r=-0.23, P<0.01) in atopics, but not in nonatopics. Apart from AMP, methacholine $PC_{20}$ was not associated with blood eosinophil markers in either group. Conclusion : Atopics more frequently displayed BHR to AMP than nonatopics. Furthermore, BHR to AMP was associated with not only blood ETCs, but serum ECP levels in atopics but was correlated with only blood ETCs in nonatopics. Those results suggest that BHR to AMP reflects airway inflammation in asthma and is more related to atopy.
Kim, Kwan-Hyoung;Oh, Yong-Seok;Kim, Chi-Hong;Kwon, Soon-Seog;Kim, Young-Kyoon;Han, Ki-Don;Moon, Hwa-Sik;Song, Jeong-Sup;Park, Sung-Hak
Tuberculosis and Respiratory Diseases
/
v.39
no.3
/
pp.219-227
/
1992
Background: Acute and chronic airway inflammation are important in the pathogenesis of bronchial asthma. Corticosteroids have proved to be very effective in the management of asthma. Although the mechanism by which they produce this effect is still debated, suppression of the inflammatory response is thought to be the most likely. Although inhaled steroids are known to be safe and have less side effects than oral steroids, the extent which inhaled steroids have beneficial and the detrimental effects in the treatment of asthma has remained open to question. Budesonide is a recently developed corticosteroid for inhalation treatment with a strong local effect combined with rapid inactivation in the systemic circulation. We set out to look in more detail at the time course of change in bronchial reactivity, clinical symptoms and the effects on the adrenal function during 6 weeks of treatment with budesonide (800 ug per day). Methods: Clinical symptoms, pulmonary function test, histamine $PC_{20}$, serum ACTH and cortisol (8 AM and 4 PM) were measured in 23 allergic asthmatic patients before and after 6 weeks of treatment with budesonide. Results: 1) Pulmonary function test; PEFR, FEV1 and FVC after 6 weeks of treatment with budesonide were higher than those before treatment. 2) Clinical symptoms; Clinical symptoms were significantly improved after 3 weeks and 6 weeks of treatment with budesonide. 3) Histamine provocation; Histamine $PC_{20}$ after 6 weeks of treatment with budesonide was significantly higher than that before treatment. 4) Adrenal function; 6 weeks of budesonide therapy did not significantly affect the level of serum ACTH and cortisol. Conclusion: From these results, it is concluded that budesonide therapy improved the clinical symptoms, pulmonary function and bronchial hyperreactivity after 3 weeks of treatment and the improvement after 6 weeks of treatment was higher than that after 3 weeks of treatment. During 6 weeks of treatment with budesonide, the inhibitory effect on the adrenal function was not obvious.
Background : Cough may be a consequence of bronchial hyperresponsiveness or inflammation. Empirical treatment is important in this context because it difficult to verify the obvious cause of cough using laboratory tests, Corticosteroid has a nonspecific anti-inflammatory effect, and can be used for cough management. However, its response rate has not yet been fully elucidated. This study investigated the short- term effects of inhaled corticosteroid on chronic cough Methods : Patients with chronic cough with a normal chest radiograph and a pulmonary function test were enrolled. Cases with a prior respiratory infection within 8 weeks, a history of bronchial asthma, objective wheezing on examination, subjective symptoms of gastroesophageal reflux or taking an ACE inhibitor were excluded. On the first visit, a methacholine bronchial provocation test, spontaneous sputum eosinophil count performed twice and a paranasal sinus radiograph were checked, and the patients were treated with budesonide turbuhaler $800{\mu}g/day$ for ten days. The primary outcome measure was a decrease in the cough score after treatment. Results : Sixty nine chronic coughers were finally analyzed. The final diagnoses by the routine tests were as follows: bronchial asthma 13.0%, eosinophilic bronchitis 18.8%, paranasal sinusitis 23.2% and non-diagnostic cases 53.6%. The following responses to the inhaled corticosteroid were observed: definite responders, 76.8%, possible responders, 2.9% and non-responders, 20.3%. The response rate was not affected by the final diagnosis even in the non-diagnostic cases. There were minimal adverse drug related effects during the empirical treatment. Conclusion : Routine objective tests such as methacholine provocation, sputum eosinophil count and simple radiographs were notare not suitable for diagnosing chronic cough Therefore, empirical treatment is important. Short term inhaled corticosteroid is effective and can guide a further treatment plan for chronic cough.
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.
BACKGROUND/OBSECTIVE: Airway inflammation by eosinophils, neutrophils and alveolar macrophages is a characteristic feature of asthma that leads to pathological subepithelial thickening and remodeling. Our previous study showed that oxidative stress in airways resulted in eosinophilia and epithelial apoptosis. The current study investigated whether glutathione-containing dry yeast extract (dry-YE) ameliorated eosinophilia, goblet cell hyperplasia and mucus overproduction. MATERIALS/METHOD: This study employed $2{\mu}g$/mL lipopolysaccharide (LPS)- or 20 ng/mL eotaxin-1-exposed human bronchial epithelial cells and ovalbumin (OVA)-challenged mice. Dry-YE employed in this study contained a significant amount of glutathione (140 mg in 100 g dry yeast). RESULTS: Human bronchial epithelial cell eotaxin-1 and mucin 5AC (MUC5AC) were markedly induced by the endotoxin LPS, which was dose-dependently attenuated by nontoxic dry-YE at 10-50 ${\mu}g$/mL. Moreover, dry-YE inhibited the MUC5AC induction enhanced by eotaxin-1, indicating that eotaxin-1-mediated eosinophilia may prompt the MUC5AC induction. Oral supplementation with 10-100 mg/kg dry-YE inhibited inflammatory cell accumulation in airway subepithelial regions with a reduction of lung tissue level of intracellular adhesion molecule-1. In addition, ${\geq}50$ mg/kg dry-YE diminished the lung tissue levels of eotaxin-1, eosinophil major basic protein and MUC5AC in OVA-exposed mice. Alcian blue/periodic acid schiff staining revealed that the dry-YE supplementation inhibited goblet cell hyperplasia and mucus overproduction in the trachea and bronchiolar airways of OVA-challenged mice. CONCLUSIONS: Oxidative stress may be involved in the induction of eotaxin-1 and MUC5AC by endotoxin episode and OVA challenge. Dry-YE effectively ameliorated oxidative stress-responsive epithelial eosinophilia and mucus-secreting goblet cell hyperplasia in cellular and murine models of asthma.
Sorbus commixta Hedl. has traditionally been used as a remedy for cough, asthma, and other bronchial disorders. In this study, three major triterpenoids-lupeol, β-sitosterol, and ursolic acid and a coumarin, scopoletin, were isolated from a CHCl3-soluble fragment of the bark of S. commixta. Their structures were identified by spectroscopic analyses, including mass spectrometry (MS), 1D-, and 2D- nuclear magnetic resonance spectroscopy (NMR), as well as by comparing the data with data reported in the literature. Scopoletin was isolated from this plant for the first time. It is a nutraceutical compound contained in many plants that has been reported to exert diverse biological activities, including anti-inflammatory effects. This study examined the inhibitory effect of scopoletin on TNF-α-induced vascular endothelial inflammation. Unlike the marginal impact of other compounds against low-density lipoprotein (LDL) oxidation and vascular endothelial inflammation, scopoletin showed remarkable activity on LDL oxidation (IC50 = 10.2 μM) and exerted vascular anti-inflammatory effects in EA.hy926 human endothelial cells activated by TNF-α. It suppressed the expression of adhesion molecules, such as ICAM-1, VCAM-1, and E-selectin, and blocked the adhesion between THP-1 monocytes and EA. hy926 endothelial cells. It also inhibited TNF-α-induced NF-κB translocation from the cytosol to the nucleus. Moreover, IκBα phosphorylation, which was increased by TNF-α treatment, was reduced after treatment with scopoletin. Thus, scopoletin inhibited TNF-α-induced vascular inflammation in endothelial cells by suppressing the NF-κB signaling pathway. These results demonstrate that owing to its anti-inflammatory activity in the vascular endothelium, scopoletin has the potential to inhibit atherosclerosis development.
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