• IMMUNE NETWORK
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• v.20 no.6
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• pp.51.1-51.17
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• 2020

Respiratory syncytial virus (RSV) causes severe pulmonary disease in infants, young children, and the elderly. Formalin inactivated RSV (FI-RSV) vaccine trials failed due to vaccine enhanced respiratory disease, but the underlying immune mechanisms remain not fully understood. In this study, we have used wild type C57BL/6 and CD4 knockout (CD4KO) mouse models to better understand the roles of the CD4 T cells and cellular mechanisms responsible for enhanced respiratory disease after FI-RSV vaccination and RSV infection. Less eosinophil infiltration and lower pro-inflammatory cytokine production were observed in FI-RSV vaccinated CD4KO mice after RSV infection compared to FI-RSV vaccinated C57BL/6 mice. NK cells and cytokine-producing CD8 T cells were recruited at high levels in the airways of CD4KO mice, correlating with reduced respiratory disease. Depletion studies provided evidence that virus control was primarily mediated by NK cells whereas CD8 T cells contributed to IFN-γ production and less eosinophilic lung inflammation. This study demonstrated the differential roles of effector CD4 and CD8 T cells as well as NK cells, in networking with other inflammatory infiltrates in RSV disease in immune competent and CD4-deficient condition.

• Tuberculosis and Respiratory Diseases
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• v.80 no.4
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• pp.325-335
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• 2017

Chronic obstructive pulmonary disease (COPD) is associated with abnormal inflammatory response and airflow limitation. Acute exacerbation involves increased inflammatory burden leading to worsening respiratory symptoms, including dyspnea and sputum production. Some COPD patients have frequent exacerbations (two or more exacerbations per year). A substantial proportion of COPD patients may remain stable without exacerbation. Bacterial and viral infections are the most common causative factors that breach airway stability and lead to exacerbation. The increasing prevalence of exacerbation is associated with deteriorating lung function, hospitalization, and risk of death. In this review, we summarize the mechanisms of airway inflammation in COPD and discuss how bacterial or viral infection, temperature, air pollution, eosinophilic inflammation, and concomitant chronic diseases increase airway inflammation and the risk of exacerbation.

• Yonsei Medical Journal
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• v.59 no.9
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• pp.1079-1087
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• 2018

Purpose: Obstructive sleep apnea and chronic obstructive pulmonary disease are independent risk factors of cardiovascular disease (CVD), and their coexistence is known as overlap syndrome (OS). Endothelial dysfunction is the initial stage of CVD; however, underlying mechanisms linking OS and CVD are not well understood. The aim of this study was to explore whether OS can lead to more severe inflammation and endothelial apoptosis by promoting endothelial dysfunction, and to assess the intervention effects of antioxidant tempol. Materials and Methods: Male Wistar rats (n=66) were exposed to normal oxygen [normal control (NC) group], intermittent hypoxia (IH group), cigarette smoke (CH group), as well as cigarette smoke and IH (OS group). Tempol intervention was assessed in OS group treated with tempol (OST group) or NaCl (OSN group). After an 8-week challenge, lung tissues, serum, and fresh blood were harvested for analysis of endothelial markers and apoptosis. Results: The levels of intracellular adhesion molecule-1, vascular cellular adhesion molecule-1, and apoptosis in circulating epithelial cells were the highest in OS group and the lowest in NC group. These levels were all greater in IH group than in CH group, and were lower in OST group than in OS and OSN groups (all p<0.001). Conclusion: Synergistic effects of IH with cigarette smoke-induced emphysema produce a greater inflammatory status and endothelial apoptosis. OS-related inflammation and endothelial cell apoptosis may play important roles in promoting cardiovascular dysfunction, and antioxidant tempol could achieve a partial protective effect.

• Journal of Physiology & Pathology in Korean Medicine
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• v.38 no.1
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• pp.16-21
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• 2024

Haepyoijin-tang and its main components have been used for phlegm, cough and dyspnea. Using a respiratory inflammation model, we intend to reveal the anti-inflammatory effect and pharmacological mechanism of Haepyoijin-tang. We induced the respiratory inflammation model by Aspergillus oryzae protease and ovalbumin administration. Female Balb/c mice (8 weeks old) were classified into four groups as follows: saline control group, aspergillus oryzae protease and ovalbumin induced respiratory inflammation group (vehicle), inflammation with Haepyoijin-tang (200 mg/kg) administration group, inflammation with dexamethasone (5 mg/kg) administration group (n=7). To identify the anti-inflammatory effects of Haepyoijin-tang water extracts, we measured the inflammatory cell number in bronchoalveolar lavage fluid (BALF) and total live lung cell number. In addition, we checked eosinophil ratio and number in BALF. And Interleukin (IL)-5 level was also measured in lung cell culture supernatant. To confirm the mechanism of anti-inflammatory effects, we analyzed the activated helper T cell (CD4⁺CD25⁺ cell) and Th2 cell (CD4⁺GATA3⁺ cell) ratio and number in lung by using flow cytometry. Finally, we attempted to confirm the immune mechanism by measuring the ratio and number of regulatory T cells (CD4⁺Foxp3⁺ cell). Haepyoijin-tang extracts treatment diminished inflammatory cell, especially, eosinophil number in BALF and total live lung cell number. Moreover, IL-5 level was reduced in Haepyoijin-tang treated group. Surprisingly, Haepyoijin-tang extracts administration not only decreased the activated helper T cell but also Th2 cell population in lung. Additionally, regulatory T cell population was increased in Haepyoijin-tang administration group. Our findings proved that Haepyoijin-tang extract have anti-inflammatory efficacy by suppressing Th2 cell activation and promoting regulatory T cell population.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.175-176
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• 2002

Airway inflammation is a characteristic of many lung disorders including asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis. All these diseases involve the recruitment of immune and inflammatory cells to the lungs leading to systemic and local chronic inflammation and oxidative stress. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.28 no.3
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• pp.229-237
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• 2024

Cough is a common symptom of several respiratory diseases. However, frequent coughing from acute to chronic often causes great pain to patients. It may turn into cough variant asthma, which seriously affects people's quality of life. For cough treatment, it is dominated by over-the-counter antitussive drugs, such as asmeton, but most currently available antitussive drugs have serious side effects. Thus, there is a great need for the development of new drugs with potent cough suppressant. BALB/c mice were used to construct mice model with cough to investigate the pharmacological effects of pectolinarigenin (PEC). Hematoxylin-eosin and Masson staining were used to assess lung injury and airway remodeling, and ELISA was used to assess the level of inflammatory factor release. In addition, inflammatory cell counts were measured to assess airway inflammation. Airway hyperresponsiveness assay was used to assess respiratory resistance in mice. Finally, we used Western blotting to explore the potential mechanisms of PEC. We found that PEC could alleviate lung tissue injury and reduce the release of inflammatory factors, inhibit of cough frequency and airway wall collagen deposition in mice model with cough. Meanwhile, PEC inhibited the Ras/ERK/c-Fos pathway to exhibit antitussive effect. Therefore, PEC may be a potential drug for cough suppression.

• The Korea Journal of Herbology
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• v.39 no.3
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• pp.77-84
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• 2024

Objectives : Lysimachia mauritiana Lam. is known as a medicinal plant native to Korea that has antioxidant, anticancer, antibacterial, and antiviral activities. However, until now, research on the cultivation technology of L. mauritiana is insufficient, and there are no research data on the systematic cultivation method and mass production of L. mauritiana. Therefore, this study aims to establish a cultivation system of L. mauritiana. Methods : The cultivation environment of open land and facilities according to the growth of L. mauritiana was compared and tested. In addition, the equivalence of the origin collection extract and the cultivation extract was evaluated through Ultra high performance liquid chromatography (UHPLC) patterns analysis according to cultivation and comparison of the effect of inhibiting respiratory inflammation using BEAS-2B human bronchial epithelial cells. Results : The cultivation technology system was established through cultivation research of L. mauritiana raw materials. In addition, as a result of comparing and evaluating the equivalence of cultivated plants and L. mauritiana raw materials for suppressing respiratory inflammation, the same results were confirmed, and the equivalence was confirmed as a result of analyzing the UHPLC pattern with L. mauritiana raw materials. Conclusions : This study suggests that extract from cultivation research of L. mauritiana plants, which are native to Korea, can be used as a health functional food or medicine to improve respiratory health.

• Journal of Society of Preventive Korean Medicine
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• v.27 no.3
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• pp.35-46
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• 2023

Objectives : Gumiganghwal-tang and its main components have been used for treatment of cough, headache, joint pain and fever. Using a respiratory inflammatory model, we intend to demonstrate the its anti-inflammatory effect and immune mechanism of Gumiganghwal-tang. Methods : We induced the respiratory inflammation mouse model by papain treatment. Female BALB/C mice (8 weeks old) were divided into three groups as follows: saline control group, papain treatment group (vehicle), papain and Gumiganghwal-tang (200 mg/kg) treatment group (n=4). To verify the anti-inflammatory effect of Gumiganghwal-tang extracts, we measured the infiltration of inflammatory cells in bronchoalveolar lavage fluid (BALF) and nasal lavage fluid (NALF). Additionally, the efficacy of Gumiganghwal-tang extracts on Th2 cell population and alveolar macrophage in lung were analyzed by using flow cytometry. Results : Gumiganghwal-tang extracts administration decreased inflammatory cell infiltration in BALF and NALF, especially of eosinophils. Furthermore, interleukin-5 level was reduced in lung by drug administration. Interestingly, Gumiganghwal-tang extracts treatment also decreased the Th2 cell (CD4⁺GATA3⁺) population and increased the alveolar macrophage (CD11b⁺CD11c⁺) population in lung. Conclusions : Our findings indicate that Gumiganghwal-tang extracts have anti-inflammatory effects by mediating Th2 cell and alveolar macrophage cell activation.

• Journal of The Korean Society of Integrative Medicine
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• v.11 no.4
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• pp.247-258
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• 2023

Purpose : This study aims to evaluate the effectiveness of a sea breeze walking program by analyzing the metabolic disease-related, immune-inflammation-related, and respiratory health-related variables of the test subjects associated with improved respiratory health. Methods : In the experiment, 30 patients with metabolic diseases were divided into an experimental group (n=15) and a control group (n=15). The experimental group walked on the Namparang-gil, Geoje trail, while the control group walked on the Hoeya-cheon, Yangsan trail. Both groups participated in the same walking program for two hours, twice a week for four weeks. Thereafter, the metabolic disease-related, immune inflammation-related, and respiratory health-related variables were measured and compared between the two groups. Results : After the four-week sea breeze walking program, in terms of changes in the metabolic disease-related variable, a statistically significant interactive effect was found in waist circumference (p<.001). The experimental group showed a significant decrease in waist circumference after the program. After the four-week sea breeze walking program, the control group showed a statistically higher increase in lactic acid (p.<05), whereas the experimental group exhibited a decrease in lactic acid. For the respiratory health-related variables, no statistically significant differences were found after the sea breeze walking program. However, the experimental group showed an increase in FEV1,while the control group showed a decrease in FEV1. For the maximum oxygen intake, no statistically significant interactive differences were found but there was a statistically significant effect in time (p<.05). The two groups exhibited an increase in maximum oxygen intake. Conclusion : After the sea breeze walking program, positive physical changes were observed in the metabolic disease-related and immune inflammation-related variables.

• Journal of Ginseng Research
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• v.47 no.1
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• pp.81-88
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• 2023

Background: Air pollution has led to an increased exposure of all living organisms to fine dust. Therefore, research efforts are being made to devise preventive and therapeutic remedies against fine dust-induced chronic diseases. Methods: Research of the respiratory protective effects of KRG extract in a particulate matter (PM; aerodynamic diameter of <4 ㎛) plus diesel exhaust particle (DEP) (PM4+D)-induced airway inflammation model. Nitric oxide production, expression of pro-inflammatory mediators and cytokines, and IRAK-1, TAK-1, and MAPK pathways were examined in PM4-stimulated MH-S cells. BALB/c mice exposed to PM4+D mixture by intranasal tracheal injection three times a day for 12 days at 3 day intervals and KRGE were administered orally for 12 days. Histological of lung and trachea, and immune cell subtype analyses were performed. Expression of pro-inflammatory mediators and cytokines in bronchoalveolar lavage fluid (BALF) and lung were measured. Immunohistofluorescence staining for IRAK-1 localization in lung were also evaluated. Results: KRGE inhibited the production of nitric oxide, the expression of pro-inflammatory mediators and cytokines, and expression and phosphorylation of all downstream factors of NF-κB, including IRAK-1 and MAPK/AP1 pathway in PM4-stimulated MH-S cells. KRGE suppressed inflammatory cell infiltration and number of immune cells, histopathologic damage, and inflammatory symptoms in the BALF and lungs induced by PM4+D; these included increased alveolar wall thickness, accumulation of collagen fibers, and TNF-α, MIP2, CXCL-1, IL-1α, and IL-17 cytokine release. Moreover, PM4 participates induce alveolar macrophage death and interleukin-1α release by associating with IRAK-1 localization was also potently inhibited by KRGE in the lungs of PM4+D-induced airway inflammation model. KRGE suppresses airway inflammatory responses, including granulocyte infiltration into the airway, by regulating the expression of chemokines and inflammatory cytokines via inhibition of IRAK-1 and MAPK pathway. Conclusion: Our results indicate the potential of KRGE to serve as an effective therapeutic agent against airway inflammation and respiratory diseases.