• Tuberculosis and Respiratory Diseases
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• 제70권3호
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• pp.235-241
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• 2011

Background: The rising prevalence of asthma may be associated with the rising prevalence of obesity in developed nations. There are several studies showing that obesity increases the risk of asthma in adults. We investigated the association of each body composition scale and bronchial hyper-responsiveness. Methods: This study involved a retrospective review of the existing records for 279 subjects with respiratory symptoms, who underwent a pulmonary function test, a methacholine challenge test and a body composition test between May 2007 and June 2009. Results: Of the 279 subjects, 179 (64%) were female. There was a statistically significant difference in fat free mass and in fat free mass index between the normal bronchial responsiveness group and bronchial hyper-responsiveness group (p=0.036; p=0.000). There was no significant differences in body mass index, in fat mass and fat free mass index in the normal bronchial responsiveness group and bronchial hyper-responsiveness group in males. However in females, body mass index and fat free mass index were increased in the bronchial hyper-responsiveness group (p=0.044; p=0.000). Total body water (kg), fat free mass (kg) and soft lean mass (kg) were significantly different between the normal bronchial responsiveness group and bronchial hyper-responsiveness group (p=0.002; p=0.000; p=0.000). Conclusion: This study showed significant differences in fat free mass and in fat free mass index between the normal bronchial responsiveness group and the bronchial hyper-responsiveness group. In females, BMI, soft lean mass, and total body water showed significant differences between the normal bronchial responsiveness group and the bronchial hyper-responsiveness group. We concluded that bronchial hyper-responsiveness was associated with not only body mass index but also fat free mass index in female bronchial asthma.

• Tuberculosis and Respiratory Diseases
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• 제80권4호
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• pp.344-350
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• 2017

Bronchial asthma is a disease characterized by the condition of airway hyper-responsiveness, which serves to produce narrowing of the airway secondary to airway inflammation and/or various spasm-inducing stimulus. Nonspecific bronchoprovocation testing is an important method implemented for the purpose of diagnosing asthma; this test measures the actual degree of airway hyper-responsiveness and utilizes direct and indirect bronchoprovocation testing. Direct bronchoprovocation testing using methacholine or histamine may have superior sensitivity as these substances directly stimulate the airway smooth muscle cells. On the other hand, this method also engenders the specific disadvantage of relatively low specificity. Indirect bronchoprovocation testing using mannitol, exercise, hypertonic saline, adenosine and hyperventilation serves to produce reactions in the airway smooth muscle cells by liberating mediators with stimulation of airway inflammatory cells. Therefore, this method has the advantage of high specificity and also demonstrates relatively low sensitivity. Direct and indirect testing both call for very precise descriptions of very specific measurement conditions. In addition, it has become evident that challenge testing utilizing each of the various bronchoconstrictor stimuli requires distinct and specific protocols. It is therefore important that the clinician understand the mechanism by which the most commonly used bronchoprovocation testing works. It is important that the clinician understand the mechanism of action in the testing, whether direct stimuli (methacholine) or indirect stimuli (mannitol, exercise) is implemented, when the testing is performed and the results interpreted.

• Tuberculosis and Respiratory Diseases
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• 제58권1호
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• pp.25-30
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• 2005

목 적 : ACE 유전자 다형성에 따라 폐를 포함한 여러 조직에서 ACE 활성 및 농도 등에 차이를 나타내고 이러한 차이가 COPD 등의 만성 호흡기 질환에서 질환의 발생 및 임상 표현형의 차이를 유발할 것으로 추정되어 지고 있다. 따라서 이 연구는 ACE 유전자 다형성이 COPD 환자에게서 동반될 수 있는 기도 과민반응 등의 기관지 천식 요소의 발현 유무와 연관성이 있는지 알아보고자 하였다. 방 법 : 100명의 COPD 환자들을 대상으로 기도 과민성의 동반 유무에 따라 두 군으로 분류하였고, PCR 방법을 통하여 ACE 유전자형을 검사하여 두 군 간의 차이를 알아보았다. 결 과 : COPD 환자에서 기도 과민반응 유무에 따른 ACE 유전자형의 분포에 차이는 없었고, COPD의 임상적 단계에 따른 각 군 간의 의미 있는 차이도 보이지 않았다. 결 론 : 이러한 연구 결과는 ACE 유전자 다형성에 따른 차이가 COPD 환자에게서 나타나는 기도 과민성 등의 천식 요소의 발현과 연관이 없음을 시사하는 소견이라 할 수 있다.

• The Korean Journal of Physiology and Pharmacology
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• 제22권5호
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• pp.481-491
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• 2018

Allergic asthma is one of the most enduring diseases of the airway. The T-helper cells and regulatory T-cells are critically involved in inflammatory responses, mucus hypersecretion, airway remodelling and in airway hyper-responsiveness. Cigarette smoke (CS) has been found to aggravate inflammatory responses in asthma. Though currently employed drugs are effective, associated side effects demand identification and development of novel drugs with negligible or no adverse effects. Rutin, plant-derived flavonoid has been found to possess antioxidant and anti-inflammatory effects. We investigated the ability of rutin to modulate T-cells and inhibit inflammation in experimentally-induced asthma in cigarette smoke exposed mice. Separate groups of neonatal mice were exposed to CS for 10 days from post-natal days 2 to 11. After 2 weeks, the mice were sensitized and challenged with ovalbumin (OVA). Treatment group were given rutin (37.5 or 75 mg/kg body weight) during OVA sensitization and challenge. Rutin treatment was found to significantly inhibit cellular infiltration in the airways and Th2 and Th17 cytokine levels as well. Flow cytometry revealed effectively raised $CD4^+CD25^+Fox3^+$ Treg cells and supressed Th17 cell population on rutin treatment. Airway hyper-responsiveness observed following CS and OVA challenge were inhibited by rutin. $NF-{\kappa}B$ and iNOS, chief regulators of inflammatory responses robustly activated by CS and OVA were down-regulated by rutin. Rutin also inhibited the expression of matrix metalloproteinase 9, thereby aiding in prevention of airway remodelling in asthma thereby revealing to be a potent candidate in asthma therapy.

• 혜화의학회지
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• 제18권1호
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• pp.1-8
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• 2009

This study analyzed the contents of the research papers of Complementary Medicine concerning the inhalation drug for asthma published in Pubmed during lately 10 years. As a result, the following conclusion was drawn. 1. There were 5 papers concerning 2 review articles, 2 experimental studies and 1 clinical study. 2. Interventions of research papers are glutathione, microorganism fermentation extract (EM-X), ginkgolide and compound Chinese herbal monomer recipe (ligustrazin, baicalin, ginkgolide). 3. There is no controlled study for effect of inhaled glutathione, on the contrary it induced bronchial constriction in sulfites sensitive asthmatics. 4. Inhalation of EM-X reduced airway hyper-reactivity and level of IL-4, IL-5 and IL-13 in OVA challenged asthmatic mice. 5. Ginkgolide nebulized inhalation reduced symptomatic scorings and eosinophil cationic protein, improved FEV1 and PEF. 6. Compound Chinese herbal monomer (CHM) recipe reduced blood eosinophil count, eosinophil count and total cell cound in BALF, depressed airway hyper-responsiveness and airway inflammation.

• Toxicological Research
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• 제30권1호
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• pp.13-18
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• 2014

Electronic cigarettes (e-cigarettes) are becoming increasingly popular worldwide and their cellular effects warrant further evaluation. In this study, we investigated the effects of an e-cigarette cartridge solution on allergen related asthmatic airway inflammation (AI) and airway hyperresponsiveness (AHR), when it is delivered by intratracheal route in mice. Asthmatic AI and AHR were induced by systemic sensitization to ovalbumin (OVA) followed by intratracheal, intraperitoneal, and aerosol allergen challenges in BALB/c mice. The cartridge solution of e-cigarette (containing 16 mg/ml nicotine) was diluted 50 times and $100{\mu}l$ of the diluted solution was intratracheally instilled to OVA-sensitized (OVA-S) mice two times a week for 10 weeks. Long-term e-cigarette inhalation elicited no remarkable changes in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase enzymes in serum, however, increased infiltration of inflammatory cells including eosinophils, into airways from blood, aggravated the asthmatic AI and AHR, and stimulated the production of cytokines such as interleukin (IL)-4, IL-5 and IL-13, and OVA-specific IgE production. Our data suggest that the inhalation of e-cigarette solutions can function as an important factor to exacerbate the allergy-induced asthma symptoms. Further studies are needed to address the effects of e-cigarette solutions on human health.

• 대한의생명과학회지
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• 제16권2호
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• pp.83-90
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• 2010

Hesperidin, a member of the flavanone group of flavonoids, can be isolated in large amounts from the rinds of some citrus species [e.g., Citrus aurantium L. (bitter orange), Citrus sinensis L. (sweet orange) and Citrus unshiu Marcov. (satsuma mandarin)], and has been reported to have anticarcinogenic, antihypotensive and antimicrobial properties. Despite the efficacy of these polyphenolic compounds as immune modulators, the effects of the flavonoids are poorly understood about allergic effect. In this study, we investigated whether hesperidin could influence on Th1 and Th2 balance. Allergic reactions included an increase in the number of eosinophils in bronchoalveolar lavage (BAL) fluid, an increase in inflammatory cell infiltration into the lung tissue around blood vessels and airways, airway luminal narrowing, the development of airway hyper-responsiveness (AHR). The administration of hesperidin before the last airway OVA challenge resulted in a significant inhibition of all asthmatic reactions. Accordingly, this study may provide evidence that hesperidin plays a critical role in the amelioration of the pathogenetic process of asthma in mice. These findings provide new insight into the immunopharmacological role of hesperidin in terms of its effects in a murine model of asthma, and also broaden current perspectives in our understanding of the immunopharmacological functions of hesperidin.

• Biomolecules & Therapeutics
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• 제32권4호
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• pp.460-466
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• 2024

Asthma is characterized by chronic inflammation and respiratory tract remodeling. Peroxisome proliferator-activated receptors (PPARs) play important roles in the pathogenesis and regulation of chronic inflammatory processes in asthma. The role of PPARγ has been studied using synthetic PPARγ agonists in patients with asthma. However, involvement of PPARα/δ has not been studied in asthma. In the present study, we investigated if elafibranor, a PPARα/δ dual agonist, can modulate ovalbumin (OVA)-induced allergic asthma, which is a potential drug candidate for non-alcoholic fatty liver in obese patients. Elafibranor suppresses antigen-induced degranulation in RBL-2H3 mast cells without inducing cytotoxicity in vitro. In mice with OVA-induced allergic asthma, the administration of elafibranor suppressed OVA-induced airway hyper-responsiveness at a dose of 10 mg/kg. Elafibranor also suppressed the OVA-induced increase in immune cells and pro-inflammatory cytokine production in the bronchoalveolar lavage fluid (BALF). Histological studies suggested that elafibranor suppressed OVA-induced lung inflammation and mucin hyper-production in the bronchial airways. In addition, elafibranor suppressed OVA-induced increases in serum immunoglobulin E and IL-13 levels in BALF. Conversely, the present study suggests that elafibranor has the potential for use in patients with allergic asthma.

• 한국식품저장유통학회지
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• 제16권2호
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• pp.253-258
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• 2009

This study investigated the effects of mycelium and culture supernatant of Cordyceps ochraceostromat(Co) on air way hyper-responsiveness, pulmonary immune cell infiltration, and Th2 cytokine expression in animal models of atopy and asthma. After ConA(+/-) activation of mouse primary spleen cells, decreased IL-4 and IL-13 cytokine production were seen in the presence of Co mycelium extracts and culture supernatant. The asthma model involved mice sensitized to ovalbumin by i.p. injection treatment; Co mycelium extract was also injected. The atopy model was the dinitrofenylbenzene-treated mouse ear. Ear thicken ing induced by DNFB was decreased by Co mycelium extract, and the extract also inhibited lung cell infiltration in ovalbumin-induced asthmatic mice. The results thus indicated that the Co mycelial extract reduced the undesirable immune responses seen in asthma and atopy.

• Tuberculosis and Respiratory Diseases
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• 제85권1호
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• pp.18-24
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• 2022

Background: Neutrophilic asthma (NeuA) is usually resistant to corticosteroids. Tiotropium bromide (TIO) is a bronchodilator that is used as an add-on therapy to inhaled corticosteroid and long-acting β2 agonist in asthma treatment. However, the role of TIO in NeuA is not fully known. Thus, the aim of this study was to evaluate the effect of TIO on NeuA compared to that of corticosteroids. Methods: C57BL/6 female mice were sensitized with ovalbumin and lipopolysaccharide to induce neutrophilic inflammation. Dexamethasone (DEX) was administered on days 14, 17, 20, and 23. TIO was inhaled on days 21, 21, and 23. On day 24, mice were sacrificed. Airway hyper-responsiveness, levels of cytokines in bronchoalveolar lavage (BAL) and lung homogenates, and lung tissue histopathology were compared between the two groups. Results: Neutrophil counts, T helper 2 cells (T_H2)/T_H17 cytokines, and pro-inflammatory cytokine in BAL fluids were elevated in the NeuA group. TIO group showed lower total cells, neutrophil counts, and eosinophil counts in BAL fluids than the DEX group (p<0.001, p<0.05, and p<0.001, respectively). Airway resistance was attenuated in the TIO group but elevated in the NeuA group (p<0.001). Total protein, interleukin (IL)-5, and IL-17A levels in BAL fluids were lower in the TIO group than in the NeuA group (all p<0.05). Conclusion: TIO showed more potent effects than DEX in improving airway inflammation and attenuating airway resistance in NeuA.