• Environmental Analysis Health and Toxicology
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• v.20 no.3 s.50
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• pp.209-213
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• 2005

Due to steady increase of childhood asthma, exposure to air toxics including PAHs have been thought as an etiology for the asthma. PAHs -involvement in airway inflammation, such as IgE production, is the potential mechanism of the PAHs-induced asthma. Cytochrome P450s (CYPs), particularly CYP1A1 is known enzyme to metabolite PAHs and to be induced by PAHs. The CYP1A1 expression has been emphasized as an biomarker for PAHs - exposure. The present study was performed to clarify the etiology of childhood asthma with PAHs-exposure using mRNA expression of CYP1A1 . The study Objects were Korean children who were asthma patients (cases) or other hospital controls (N=20; age,3 $\~$ 16; boys,56$\%$). As result, we detected expression of the CYP1A1 in all peripheral blood specimens which were collected from the subjects. Moreover, we found approx. 300 fold-higher expression of the CYP1A1 in the cases than that in the controls (p(<)0.01). When we considered age which was related to Asthma, the above significant trend was somewhat diluted, however, the relation between asthma and the Cypih i expression waL stronger than that between asthma and age (chi square,7.99 vs. 3.34). Therefore, our study supports that PAHs induce or worse childhood asthma and suggests application of expression of the CYP1A1 as an initiation or progress biomarker for PAHs - induced childhood asthma.

• Toxicological Research
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• v.17 no.4
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• pp.255-265
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• 2001

Epidemiologic studies have demonstrated an association between short-term exposure to particulate air pollutants and increased mortality. However the biological mechanism underlying these associations have not been fully established and also the chemical and physical characteristics of the pollutant particles are not well understood. The metal constituents of air pollutant particles and their bioavailability are considered to Play an important role as possible mediators of Particle-induced airway injury and inflammation. Sprague-Dawley rat alveolar macrophage cells (NR8383) were exposed to airborne and acid-leached particulate matter (PM). Titanium oxide and nickel subsulfide were used as negative and positive controls. Particle-induced reactive oxygen species formation in cells was detected using the fluorescent probe 2',7'-dichlorofluorescin diacetate. Expression of TNF-$\alpha$ and IL-6 were measured by enzyme-linked immunosorbent assay, and PM-induced DNA double-strand breaks were determined with $\lambda$DNA/Hind III marker. Metals associated with air pollutant particles mediated intracellular oxidant production in alveolar macrophages, and the cytotoxicity and proinflammatory cytokine production induced by PM were associated with oxidative stress. The oxidants produced by air pollutant particles also are likely to induce DNA double-strand breaks. Our findings in alveolar macrophage cells exposed to PM and acid-leached PM support the hypothesis that metal components in urban air pollutants and their bioavailabilities might play an Important role in the induction of the adverse health effects.

• Korean Journal of Bronchoesophagology
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• v.4 no.2
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• pp.182-187
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• 1998

Platelet activating factor (PAP) has been known as implicating as one of potent inflammatory mediators and reported 0 be involved in inflammation and allergy. PAF induces ciliary dysfunction and epithelial damage of human paranasal sinus mucosa in vitro. However, several recent papers have reported that PAF may not readily damage the airway epithelium. The aim of this study was to investigate the ultrastructural evidence to elucidate the pathogenesis of epithelial damage induced by PAF. Sixteen $\mu\textrm{g}$ g of PAF was applied into the maxillary sinuses of 6 rabbits. Rabbits were divided into 2 subgroups along with time interval at 1st and 3rd experimental day, and sinus mucosae were taken for the histopathologic study using electron microscopy. At 1st day, epithelial cells showed no ultrastructural change. Ultrastructures of the cilia were well preserved. Subepithelial space showed no evidence of the infiltration of inflammatory cells. Intravascular platelet aggregation and swelling of endothelial cells were evident. At 3rd day, epithelial cells showed vacuolar degeneration. Fusion of cilia forming giant cilia and focal loss of cilia were evident. Eosinophils were infiltrated in subepithelial and intraepithelial space. Swelling of endothelial cells, and migration of inflammatory cells into the connective tissue were evident. This study implies that epithelial damage induced by PAF may be secondary to the cytotoxicity of mobilized eosinophils rather than direct cytotoxicity of PAF.

• Korean Journal of Bronchoesophagology
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• v.7 no.1
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• pp.5-8
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• 2001

Background and Objectives： Complications arising from endotracheal intubation are uncommon but, when they do occur, can be significant. Placement of an endotracheal tube frequently results in trauma to the underlying laryngeal and tracheal tissue, although the trauma is usually reversible. Occasionally, these changes can be of a more permanent nature and result in severe impairment of the airway and/or voice. It is proposed that a common factor-gastroesophageal reflux-might be responsible. This study was performed in order to develop the animal model of LPRD using rats and investigated that LPRD could produce significant damage to larynx especially vocal cords. Materials and Methods : The each four rats were used in the experiment and control study. Each was anesthetized and larynx was exposed and injured in the unilateral aritenoid. Injured site was contact with normal saline(control group) and synthetic gastric juice(experimental group). The larynx was examined after 7days in normal environment. Results : All was survived in the control group and two was survived in the experimental group. In the control group, some inflammation cells was found but in the experimental group, granulation was found. Conclusion : We developed animal model of LPRD using rat and thought LPRD may Play an important role in the development of permanent laryngeal injury.

• Journal of Oral Medicine and Pain
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• v.43 no.3
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• pp.61-69
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• 2018

Obstructive sleep apnea (OSA) is a relatively common, but greatly underdiagnosed sleep-related breathing disorder, characterized by recurrent collapse of the upper airway during sleep. OSA has been associated with a variety of cardiometabolic disease, such as hypertension, coronary artery disease, cardiac arrhythmia, cerebrovascular disease and metabolic dysfunction. Neurocognitive impairment, including excessive daytime sleepiness, increased risk of motor vehicle accidents, is also related to OSA. Sleep fragmentation and related arousals during sleep lead to intermittent hypoxia, sympathetic activation, oxidative stress, systemic inflammation and metabolic dysregulation which provide biological plausibility to this pathologic mechanism. Extensive studies demonstrated that OSA is a modifiable risk factor for the above mentioned diseases and oral appliances (OAs), although continuous positive air pressure (CPAP) is a first-line therapy of OSA, are not inferior to CPAP at least in mild OSA, and may be an alternative to CPAP in CPAP-intolerant subjects with OSA. The goal of this article is to provide a current knowledge of pathologic link between OSA and cardiovascular disease, focusing on intermittent hypoxia, sympathetic activation, oxidative stress and metabolic dysregulation. Then, previous epidemiologic studies will be reviewed to understand the causal relationship between OSA and cardiovascular disease. Finally, the effects of OAs will be updated via recent metaanalyses compared to CPAP.

• Tuberculosis and Respiratory Diseases
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• v.85 no.4
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• pp.289-301
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• 2022

Chronic obstructive pulmonary disease (COPD) is a chronic airway inflammation characterized by fixed airflow limitation and chronic respiratory symptoms, such as cough, sputum, and dyspnea. COPD is a progressive disease characterized by a decline in lung function. During the natural course of the disease, acute deterioration of symptoms leading to hospital visits can occur and influence further disease progression and subsequent exacerbation. Moreover, COPD is not only restricted to pulmonary manifestations but can present with other systemic diseases as comorbidities or systemic manifestations, including lung cancer, cardiovascular disease, pulmonary hypertension, sarcopenia, and metabolic abnormalities. These pulmonary and extrapulmonary conditions lead to the aggravation of dyspnea, physical inactivity, decreased exercise capacity, functional decline, reduced quality of life, and increased mortality. In addition, pneumonia, which is attributed to both COPD itself and an adverse effect of treatment (especially the use of inhaled and/or systemic steroids), can occur and lead to further deterioration in the prognosis of COPD. This review summarizes the long-term outcomes of patients with COPD. In addition, recent studies on the prediction of adverse outcomes are summarized in the last part of the review.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2020.12a
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• pp.3-13
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• 2020

Pseudomonas aeruginosa is a ubiquitous gram-negative bacterium causing serious infections. The P. aeruginosa T3SS is a syringe-like apparatus on the bacterial surface, with 4 effector toxins: ExoS, ExoT, ExoY, and ExoU. Here, we investigated the effect of ExoS and ExoT of the T3SS of P. aeruginosa K strain (PAK). The type three secretion system (T3SS) is a major virulence system of Pseudomonas aeruginosa (P. aeruginosa). The effector protein Exotoxin S (ExoS) produced by P. aeruginosa is secreted into the host cells via the T3SS. For the purpose of screening the inhibitors with regard to ExoS secretion, we developed the sandwich-type enzyme-linked immunosorbent assay (ELISA) system. PAK clinical strains induce proinflammatory cytokine production through the T3SS, and this involves NF-κB activation in pneumonia mouse models. We tried to confirm the role of the NF-κB transcription factor in ExoS- and ExoT-induced pneumonia mouse models. pro-inflammatory cytokines induction in response to ExoS and ExoT infection relied on NF-κB activation. Our findings highlight the roles of natural poduct in inhibiting proinflammatory cytokine expression during ExoS and ExoT exposure in PAK infections, paving the way for a novel therapeutic approach for the treatment of pulmonary infections.

• The Journal of Korean Medicine
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• v.44 no.3
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• pp.163-169
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• 2023

Objectives: This study aimed to review the experimental research trends in asthma caused by particulate matter to conduct further researches, especially in clinical trials. Methods: We searched for the meaningful literature using medicinal herb for asthma through the Pubmed databases. Results: Finally, six studies were finally selected. These studies showed recent trends, from 2018 to 2021 and conducted mostly in South Korea. The type of fine dust and the method of inducing asthma are different for each paper, but the effective mechanism is relatively common. It was commonly confirmed that the ratio and number of eosinophils, th2 cells and related cytokines are decreased in BALF and lung tissue by administration of medicinal herb. Conclusions: Although the method of inducing asthma using fine dust has not yet been standardized, it is thought that more meaningful evaluation results can be derived if a standardized animal model is established in the future. Nevertheless, based on the results that herbal medicine is effective for particular matter induced asthma, it is expected that it will be the basis for expanding into future clinical studies.

• Clinical and Experimental Pediatrics
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• v.51 no.2
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• pp.181-187
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• 2008

Purpose : Asthma is characterized by reversible airway obstruction and bronchial hyperresponsiveness result from airway inflammation. Fraction of nitric oxide in expired air (FeNO) has recently been investigated as a noninvasive measure of airway inflammation. FeNO has been reported to correlate with induced sputum eosinophilia and methacholine challenge test that it is represent severity of asthma. The purpose of this study was to analyze the relationship of FeNO with pulmonary function tests in patients with intermittent asthma. Methods : Eighty children included in this study were diagnosed as asthma from April through August, 2005 in Department of Pediatrics, College of Medicine, Kyunghee University. They aged from 4 to 15 years who were able to conduct spirometry and FeNO monitoring. They did not have upper respiratory tract infection and did not use an asthma controller which contain corticosteroids within 4 weeks. Pulmonary function test was done and FeNO was measured with online tidal breathing method using a chemiluminescence NO analyzer (CLD 88 sp, Eco Medics, Duernten, Switzerland). The correlations between pulmonary function test and FeNO were analyzed using Spearman correlation coefficient method. Results : The mean of FeNO of subject was 16.88 parts per billion (ppb). The mean of forced expiratory volume in 1 second ($FEV_1$) was $0.890{\pm}0.455L$ and forced vital capacity (FVC) was $1.071{\pm}0.630L$. The mean of predicted $FEV_1%$ ($FEV_1%pred$) was $98.39{\pm}34.27%$ and $FEV_1/FVC$ was $88.53{\pm}19.49$. FeNO was significantly correlate with $FEV_1$ (r=0.345, P<0.01) and FVC (r=0.244, P<0.05). FeNO did not correlate with $FEV_1%pred$ or $FEV_1/FVC$. Conclusion : The measurement of FeNO could be a useful marker in the management of childhood asthma and it is evolving to provide a complementary role alongside existing pulmonary function test. We propose that measuring technique and establishment of normal reference range are important area for future research.

• Tuberculosis and Respiratory Diseases
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• v.54 no.1
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• pp.104-113
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• 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.