• The Korea Journal of Herbology
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• v.26 no.4
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• pp.49-57
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• 2011

Objective : Allergic asthma is a chronic airway disease that affects millions of people in the developed world. The disease is characterized by concurring airway inflammation, Th2 cytokine production, increased mucus secretion, airway hyperresponsiveness (AHR) to inhaled antigen, and pulmonary fibrosis. To investigate the therapeutic and anti-asthmatic effects of Drynariae Rhizoma (DR), we examined the influence of DR on the development of pulmonary eosinophilic inflammation and airway hyperresponsiveness in a mouse model of allergic asthma. Methods : In this study, BALB/c mice were systemically sensitized to ovalbumin (OVA) followed intratracheally, intraperitoneally, and by aerosol allergen challenges. We investigated the effect of DR on airway hyperresponsiveness, pulmonary eosinophilic infiltration, various immune cell phenotypes, Th2 cytokine production and OVA specific IgE production in a mouse model of asthma. Results : In asthmatic mice, we found that DR.treated groups had suppressed eosinophil infiltration, allergic airway inflammation and AHR by suppressing the production of IL-5, IL-13 and OVA specific IgE. Conclusions : Our data suggest that the therapeutic mechanism by which DR effectively treats asthma is based on reductions of Th2 cytokines (IL-5), eotaxin, OVA-specific IgE production and eosinophil infiltration.

• Journal of Society of Preventive Korean Medicine
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• v.10 no.2
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• pp.121-129
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• 2006

BACKGROUND : Socheongryong-Tang(小靑龍湯, SCRT), a herbal medicine, has been widely used for the control of respiratory disease in Eastern countries. Recent years SCRT was known as anti-allergic agent. However, its therapeutic mechanisms, especially an inhibitory effect on inflammatory cell infiltration and airway remodeling in allergic asthma are unclear. METHODS : We investigated the effects of SCRT on levels of IL-4, and IFN-g using flow cytometric analysis and infiltration of inflammatory cells in bronchoalveolar lavage fluid(BALF) using cytospin methods in allergen-induced asthma. RESULTS : SCRT decreased levels of IL-4, a Th2-driven cytokine. But INF-g, a Th1-driven cytokine, was not changed. With SCRT treatment, infiltration of inflammatory cells showed reduced tendency. CONCLUSION : In conclusion, we demonstrated that regulation of Th1/Th2 imbalance may be one of mechanism contributed to reduction of inflammatory cell infiltration.

• IMMUNE NETWORK
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• v.11 no.3
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• pp.169-174
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• 2011

Background: NADPH oxidase (NOX) modulates cell proliferation, differentiation and immune response through generation of reactive oxygen species. Particularly, NOX2 is recently reported to be important for regulating Treg cell differentiation of CD4+ T cells. Methods: We employed ovalbumin-induced airway inflammation in wild-type and NOX2-deficient mice and analyzed tissue histopathology and cytokine profiles. Results: We investigated whether NOX2-deficiency affects T cell-mediated airway inflammation. Ovalbumin injection which activates T cell-mediated allergic response increased airway inflammation in wild-type mice, as evidenced by increased immune cell infiltration, allergic cytokine expression, and goblet cell hyperplasia in the lung. Interestingly, NOX2 knockout (KO) mice were more susceptible to allergen-induced lung inflammation compared to wild-type mice. Immune cells including neutrophils, lymphocytes, macrophages, and eosinophils were drastically infiltrated into the lung of NOX2 KO mice and mucus secretion was substantially increased in deficiency of NOX2. Furthermore, inflammatory allergic cytokines and eotaxin were significantly elevated in NOX2 KO mice, in accordance with enhanced generation of inflammatory cytokines interleukin-17 and interferon-${\gamma}$ by CD4+ T cells. Conclusion: These results indicate that NOX2 deficiency favorably produces inflammatory cytokines by T cells and thus increases the susceptibility to severe airway inflammation.

• Clinical and Experimental Pediatrics
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• v.56 no.11
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• pp.482-489
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• 2013

Purpose: The aim of the present study was to investigate the differences in lower airway inflammatory immune responses, including cellular responses and responses in terms of inflammatory mediators in bronchoalveolar lavage fluid (BALF) and the airway, to rhinovirus (RV) infection on asthma exacerbation by comparing a control and a murine asthma model, with or without RV infection. Methods: BALB/c mice were intraperitoneally injected with a crude extract of Dermatophagoides farinae (Df ) or phosphate buffered saline (PBS) and were subsequently intranasally treated with a crude extract of Df or PBS. Airway responsiveness and cell infiltration, differential cell counts in BALF, and cytokine and chemokine concentrations in BALF were measured 24 hours after intranasal RV1B infection. Results: RV infection increased the enhanced pause (Penh) in both the Df sensitized and challenged mice (Df mice) and PBS-treated mice (PBS mice) (P<0.05). Airway eosinophil infiltration increased in Df mice after RV infection (P<0.05). The levels of interleukin (IL) 13, tumor necrosis factor alpha, and regulated on activation, normal T cells expressed and secreted (RANTES) increased in response to RV infection in Df mice, but not in PBS mice (P<0.05). The level of IL-10 significantly decreased following RV infection in Df mice (P<0.05). Conclusion: Our findings suggest that the augmented induction of proinflammatory cytokines, Th2 cytokines, and chemokines that mediate an eosinophil response and the decreased induction of regulatory cytokines after RV infection may be important manifestations leading to airway inflammation with eosinophil infiltration and changes in airway responsiveness in the asthma model.

• Journal of Korean Society for Atmospheric Environment
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• v.24 no.3
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• pp.321-328
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• 2008

The number of patient with allergic asthma and atopy have increased in the cities of Korea steadily. In order to elucidate the primary factor, we investigated whether the house dust particles collected from an apartment of the middle classes has promoting effects of allergen-related airway inflammation and airway hyperresponsiveness. Mice were treated with 0.1 mL of 1 mg/mL of house dust particles suspension by intratracheal instillation once weekly for 10 weeks combined with ovalalbumin (OVA) sensitization. Intratracheal instillation of house dust particles and OVA sensitization caused an increase in the level of serum L-lactate dehydrogenase (LDH), immunoglobulun-E (IgE) and histamine, and an elevation in respiratory resistance. It also enhanced infiltration of eosinophils in the bronchoalveolar lavage fluid (BALF) of mice, IgE and eotaxin expression in blood, and T helper type 2 cell derived cytokine levels such as of interleukin (IL)-4, IL-13 and IL-5 in the BALF. However, it did not influence T helper type 1 cytokine such as interferon-gamma in the BALF. These results indicate that house dust particles elevate allergen-related airway inflammation and airway hyperresponsiveness in mice and may play an important role in the aggravation of asthma and atopy in Korea.

• 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.

• Korean Journal of Medicinal Crop Science
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• v.25 no.5
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• pp.269-281
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• 2017

Background: Small particles increase airway inflammation upon reaching the alveoli. Here, we investigated the protective or therapeutic effects of Salvia plebeia R. Br. (SP_R) extracts on airway inflammation. Methods and Results: To investigate the anti-inflammatory activity of SP_R extracts, we measured their inhibitory effect on the production of reactive oxygen species (ROS) expression of inflammatory mediators, and immune cell infiltration in MH-S alveolar macrophage cells and in the ambient particulate matter (APM)-exposed airway inflammation mice model. The SP_R extracts inhibited the production of ROS and expression of IL-4, IL-10, IL-15, and IL-17A mRNA in APM-stimulated MH-S cells. Oral administration of SP_R extracts suppressed APM-induced inflammatory symptoms, such as high alveolar wall thickness, excess collagen fibers, decreased mRNA expression of chemokines (Ccr9, Ccl5, Ccr3), inflammatory cytokines (IL-15, TNF-${\alpha}$), and IL-4 Th2 cytokine in the lung. The SP_R extracts also inhibited ROS production, granulocyte ($CD11b^+Gr-1^+$) infiltration, IL-17A, TNF-${\alpha}$, macrophage inflammatory protein (Mip-2), and chemokine (C-X-C motif) ligand 1 (Cxcl-1) production in the airway. The specific compounds in the SR-R extracts that mediate the anti-inflammatory effects were identified. Conclusions: In this study, SP_R extracts effectively inhibited airway inflammatory responses, such as ROS production and granulocyte infiltration into the airway, by regulating the expression of chemokines and inflammatory cytokines.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.32 no.2
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• pp.1-10
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• 2019

Objectives : The objective of present study is to evaluate anti-inflammatory and anti-allergic effects of Perilla(Perilla frutescens; Labiatae, PF), the roots of Peucedanum praeruptorum(PP) and the root of Scutellaria baicalensis(SB) in vitro and anti-asthmatic effects of mixture of PF, PP and SB(PS) on ovalbumin (OVA)-induced asthma in BALB/c mice. Methods : Anti-inflammatory and anti-allergic effects were observed on the lipopolysaccharide(LPS) treated RAW 264.7 cells through Nitric Oxide(NO) production and RBL-2H3 cells through ${\beta}$-hexosaminidase. Anti-asthmatic effects were observed on the number of inflammatory cells in bronchoalveolar lavage fluid(BALF) and the level of IgE in serum on OVA-induced BALB/c mice. Results : The treatment of PF, PP and SB(12.5, 25, 50, $100{\mu}g/m{\ell}$) resulted in a significant inhibition of NO production in RAW 264.7 cells and mast cell degranulation in RBL-2H3 cells. Oral administration of PS(400mg/kg/day) resulted in a significant reduction in the numbers of eosinophils in BALF and level of IgE in serum. Conclusion : The oral administration of PS is effective in ameliorating the eosinophilic infiltration in vivo and thus can be a good therapeutic candidate for allergic asthma.

• Korean Journal of Medicinal Crop Science
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• v.17 no.2
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• pp.90-96
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• 2009

The objective of this study was to investigate the effect of crude ginseng total saponins (CGS) against airway inflammation (AI) and airway hyperresponsiveness (AH) induced by diesel exhaust particles (DEP) in mice. AI and AH were induced by the intratracheal instillation with 0.1 $mg/m{\ell}$ of DEP suspension once a week for 10 weeks combined with ovalbumin (OVA) sensitization. Mice were also treated orally with 75 $mg/m{\ell}$ of CGS, 5 days a week for 10 weeks. Oral CGS treatment decreased in the level of serum immunoglobulin (IgE) and histamine increased by DEP and OVA, and declined respiratory resistance. It also dropped an enhanced infiltration of eosinophils in the bronchoalveolar lavage fluid (BALF) of mice, and an increased T helper type 2 cell derived cytokine levels such as of interleukin (IL)-4, IL-13 and IL-5 in the BALF. However, it did not influence T helper type 1 cytokine such as interferon-gamma in the BALF. These results indicate that CGS may alleviate allergen-related AI and AH in mice and may play an important role in the modulation of asthmatic inflammation.

• 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.