• Proceedings of the PSK Conference
• /
• 2003.04a
• /
• pp.210.2-211
• /
• 2003

Eosinophilic inflammation is the main histological correlate of airway hyperresponsiveness and tissue injury in the pathogenesis of bronchial asthma. Interleukin (IL)-5 appears to be one of main proinflammatory mediators that induce eosinophilic inflammation. Allergic IL -5-deficient mice do not generate eosinophilia in the bone marrow, blood or lung in response to allergen provocation. (omitted)

• IMMUNE NETWORK
• /
• v.10 no.4
• /
• pp.109-114
• /
• 2010

The molecular mechanisms involved in the pathogenesis of chronic obstructive pulmonary disease (COPD) are poorly defined. Accumulating evidences indicate that chronic inflammatory responses and adaptive immunity play important roles in the development and progression of the disease. Recently, it has been shown that IL-17 producing CD4 T cells, named Th17 cells, which have been implicated in the pathogenesis of several inflammatory and autoimmune diseases, are involved in airway inflammation and COPD. In addition, we and others suggest that autoimmunity may play a critical role in the pathogenesis of COPD. Here, we will review the current understanding of roles of Th17 cells and autoimmune responses in COPD.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.19 no.3
• /
• pp.612-617
• /
• 2005

Astragali Radix(AR), is a popular tonic herb prescribed for 'insufficient qi' in Korea, Japan and China. The present study examined the effect of AR ethanol extract on ovalubumin induced allergic mouse model. AR administration reduced levels of IFN-gamma, Interleukin(IL)-4, IL-5 and total IgE in the OVA induced allergic inflammation. It also protected the upper airway respiratory epithelium from being damaged by the OVA induced inflammation. Taken together, our results showed that the use of AR alone proved to down-regulate Th1 and Th2 cytokine production and play a protective role in tissue damage in allergic disease.

• Tuberculosis and Respiratory Diseases
• /
• v.85 no.3
• /
• pp.221-226
• /
• 2022

Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation due to chronic airway inflammation and destruction of the alveolar structure from persistent exposure to oxidative stress. The body has various antioxidant mechanisms for efficiently coping with such oxidative stress. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) is a representative system. Dysregulation of the Nrf2-ARE pathway is responsible for the development and promotion of COPD. Furthermore, COPD severity is also closely related to this pathway. There has been a clinical impetus to use Nrf2 for diagnostic and therapeutic purposes. Therefore, in this work, we systematically reviewed the clinical significance of Nrf2 in COPD patients, and discuss the value of Nrf2 as a potential COPD biomarker.

• Tuberculosis and Respiratory Diseases
• /
• v.86 no.3
• /
• pp.151-157
• /
• 2023

The introduction of inhaled corticosteroids (ICS) for the management of asthma has led to a decrease in acute exacerbation of asthma. However, there are concerns regarding the safety of long-term ICS use, particularly pneumonia. Growing evidence indicates that ICS use is associated with an increased risk of pneumonia in patients with chronic obstructive pulmonary disease, whereas the risk in patients with asthma remains unclear. This review discusses the effect of ICS on pneumonia among patients with asthma to update the existing literature. Asthma is associated with an increased risk of pneumonia. Several hypotheses have been proposed to explain this association, including that asthma impairs the clearance of bacteria owing to chronic inflammation. Therefore, controlling airway inflammation with ICS may prevent the occurrence of pneumonia in asthma. In addition, two meta-analyses investigating randomized control trials showed that ICS use was associated with a protective effect against pneumonia in asthma.

• Tuberculosis and Respiratory Diseases
• /
• v.43 no.3
• /
• pp.420-433
• /
• 1996

Background : There have been many debates about the effects of nitric oxide on the neurogenic inflammation. The role of nitric oxide in the neurogenic inflammation of airways will be required a better understanding of the localization and types of nitirc oxide synthase(NOS) activity in the neurogenic inflammation of airways. Method : To investigate the role of nitric oxide in airway neurogenic inflammation, 1) the effects of neurokinin receptor antagonist (FK224) and nitric oxide synthase inhibitor, $N^{\omega}$-nitro-L-arginine (L-NNA) on plasma extravastion were evaluated in four groups of Sprague-Dawley rats ; sham operation group(sham NANC group), electrical vagal stimulation group(NANC2 group), intravenous pretreatment groups with FK224 (1mg/kg ; FK224 group), and L-NNA(1mg/kg ; L-NNA group) 15 minutes before vagal NANC stimulation. 2) NOS activity in trachea with neurogenic inflammation was localized by immunohistochemical stain. Immunohistochemical stain was performed by antibodies specific for inflammatory cells(iNOS), brain(bNOS), and endothelium (eNOS) on trachea obtained from sham NANC, NANC2, and FK224 groups. Results : The results are that plasma extravsation in neurogenic inflammation of rat airways was inhibited by FK224, but enhanced by L-NNA pretreatment(P<0.05). There was significantly increased infiltration of inflammatory cells in subepithelium of neurogenic inflammatory trachea, but the reduction of subepithelial infiltration of inflammatory cells was observed after pretreatment with FK224(P<0.05). Immunostaining with anti-iNOS antibody showed strong reactivity only in infiltrated inflammatory cells in neurogenic rat trachea, and these iNOS reactivity was reduced by pretreatment with FK224. bNOS immunoreactivity was significantly increased only in the nerves both of neurogenic inflammatory and FK224 pretreated trachea compared with sham NANC trachea(p<0.05). eNOS immunoreactivity was not significant change in endothelium in neurogenic inflammation of rat trachea. Conclusion : These results suggest that nitric oxide released from iNOS in infiltrated inflammatory cells has main role in neurogenic inflammation of rat trachea. The presence of bNOS immunoreactivity in the nerves indicates that nitric oxide may be released from the nerves in rat trachea with neurogenic inflammation.

• The Journal of Internal Korean Medicine
• /
• v.26 no.1
• /
• pp.199-212
• /
• 2005

Objective : Airway inflammation is now regarded as a defining feature of asthma. The importance of eosinophits in the airway inflammation of asthma patients is widely recognized, and eosinophils mobilization in the respiratory epithelium is activated by chemoattractants and cytokines. This study was designed to examine the extent of the ability of Moutan Cortex Radicis to inhibit eosinophil chemotaxis of pulmonary epithelium after allergic stimulation. Material and Methods : Water extracts of Moutan Cortex Radicis and pulmonary epithelial cell lines A549(human type II-like epithelial cells) and human eosinophils were used. Cytotoxic effects of Moutan Cortex Radicis were estimated via MTS assay, and the effects of Moutan Cortex Radicis on chemokines from prestimulated A549 cells were estimated by sandwich ELISA and RT-PCR. Chemotaxis assay on prestimulated eosinophils treated with Moutan Cortex Radicis. was conducted Result : In this study we demonstrated that $TNF-{\alpha}$ and IL-4, $IL-1{\beta}$ induced the accumulation of chemokines' mRNA in the pulmonary epithelial cell lines A549 in a dose-dependent manner. Chemokines of eotaxin, ICAM-1, YCAM-1, IL-8, IL-16 were inhibited by Moutan Cortex Radicis in a dose dependent manner, but RANTES showed no inhibition due to Moutan Cortex Radicis. Eosinophil migration was inhibited at high concentrations of Moutan Cortex Radicis. Conculusion : These findings are indicative of supression of chemokines accomplished by Moutan Cortex Radicis treatment, demonstrating the potential therapeutic value of Moutan Cortex Radicis for treating diseases such as asthma.

• Tuberculosis and Respiratory Diseases
• /
• v.46 no.6
• /
• pp.861-868
• /
• 1999

Relapsing polychondritis (RP) is a rare inflammatory disorder of unknown etiology, causing recurrent inflammatory and degenerative reactions involving the cartilaginous structures throughout the body. Generally, RP is known as multiorgan disease presented as auricular chondritis, arthritis, nasal chondritis, ocular inflammation, audiovestibular damage and respiratory tract inflammation. Major airway involvement occurs in more than 50% of the patient and has been reported to be the primary cause of death. Rarely, it may be presented with only respiratory symptoms without typical clinical manifestation of RP. We experienced a 64-year-old male patient with RP involving diffuse airway tract without other characteristic clinical manifestation and present here with a review of literatures.

• Laboraroty Animal Research
• /
• v.33 no.1
• /
• pp.40-47
• /
• 2017

HemoHIM, herbal preparation has designed for immune system recovery. We investigated the anti-inflammatory effect of HemoHIM on cigarette smoke (CS) and lipopolysaccharide (LPS) induced chronic obstructive pulmonary disease (COPD) mouse model. To induce COPD, C57BL/6 mice were exposed to CS for 1 h per day (eight cigarettes per day) for 4 weeks and intranasally received LPS on day 26. HemoHIM was administrated to mice at a dose of 50 or 100 mg/kg 1h before CS exposure. HemoHIM reduced the inflammatory cell count and levels of tumor necrosis factor receptor (TNF)-${\alpha}$, interleukin (IL)-6 and IL-$1{\beta}$ in the broncho-alveolar lavage fluid (BALF) induced by CS+LPS exposure. HemoHIM decreased the inflammatory cell infiltration in the airway and inhibited the expression of iNOS and MMP-9 and phosphorylation of Erk in lung tissue exposed to CS+LPS. In summary, our results indicate that HemoHIM inhibited a reduction in the lung inflammatory response on CS and LPS induced lung inflammation via the Erk pathway. Therefore, we suggest that HemoHIM has the potential to treat pulmonary inflammatory disease such as COPD.

• Tuberculosis and Respiratory Diseases
• /
• v.85 no.1
• /
• pp.67-73
• /
• 2022

Background: Bronchiectasis patients with neutrophilic airway inflammation develop symptoms of chronic cough, sputum production, and recurrent exacerbations. Roflumilast has anti-inflammatory actions via decreased neutrophilic airway inflammation. The effectiveness of roflumilast to reduce bronchiectasis exacerbation has never been evaluated. Methods: We conducted a double-blinded, randomized, placebo-controlled trial. Our primary objective was to assess the effect of roflumilast compared with that of a placebo in reducing exacerbation rates in bronchiectasis patients. The secondary objectives were the changes in forced expiratory volume in 1 second (FEV₁) and St. George's Respiratory Questionnaire (SGRQ). Bronchiectasis patients older than 18 years who had had two exacerbations during the previous 12 months were randomly assigned to receive either 500 ㎍ of either roflumilast or a placebo once daily for 6 months in a 1:1 ratio. Results: Forty bronchiectasis patients who had experienced exacerbations were screened. Thirty patients completed the study after 6 months of treatment: roflumilast group (n=15) and placebo group (n=15). The rates of exacerbations were 0.57 and 0.59 per patient in the roflumilast and placebo groups, respectively. Prebronchodilator FEV₁ increased by 0.07 L from baseline in the roflumilast group and decreased by 0.015 L in the placebo group, but the difference was not significant. No significant differences were observed in the change of SGRQ scores between the roflumilast and placebo groups. Roflumilast had significant side effects, including loss of appetite and headache. Conclusion: Roflumilast did not significantly affect the rate of exacerbations or quality of life. However, FEV₁ tended to improve more in the roflumilast group than in the placebo group.