• Tuberculosis and Respiratory Diseases
• /
• v.60 no.6
• /
• pp.608-624
• /
• 2006

• Clinical and Experimental Pediatrics
• /
• v.53 no.2
• /
• pp.121-128
• /
• 2010

In recent years, environmental tobacco smoke (ETS) has become an important worldwide public health issue. Children are particularly vulnerable to ETS because they are still developing. ETS exposure causes a wide range of adverse health effects on childhood asthma. There is convincing evidence that ETS exposure is causally associated with an increased prevalence of asthma, increased severity of asthma and worsening asthma control in children who already have the disease, even though a causal relationship with asthma onset is not yet established for asthma incidence. Mechanisms underlying these adverse effects of ETS are not clearly elucidated but e studies on this issue suggest that genetic susceptibility, impaired lung function, and augmented airway inflammation and remodeling may be involved. Children with asthma are just as likely to be exposed to ETS as children in general and there is no risk-free level of exposure. Therefore, providing a smoke-free environment may be of particular importance to the asthmatic children exposed to ETS who have adverse asthma outcomes, as well as to children with genetic susceptibility who are at increased risk of developing asthma upon exposure to ETS in early childhood.

• IMMUNE NETWORK
• /
• v.19 no.1
• /
• pp.5.1-5.12
• /
• 2019

Autophagy is a homeostatic mechanism that discards not only invading pathogens but also damaged organelles and denatured proteins via lysosomal degradation. Increasing evidence suggests a role for autophagy in inflammatory diseases, including infectious diseases, Crohn's disease, cystic fibrosis, and pulmonary hypertension. These studies suggest that modulating autophagy could be a novel therapeutic option for inflammatory diseases. Eosinophils are a major type of inflammatory cell that aggravates airway inflammatory diseases, particularly corticosteroid-resistant inflammation. The eosinophil count is a useful tool for assessing which patients may benefit from inhaled corticosteroid therapy. Recent studies demonstrate that autophagy plays a role in eosinophilic airway inflammatory diseases by promoting airway remodeling and loss of function. Genetic variant in the autophagy gene ATG5 is associated with asthma pathogenesis, and autophagy regulates apoptotic pathways in epithelial cells in individuals with chronic obstructive pulmonary disease. Moreover, autophagy dysfunction leads to severe inflammation, especially eosinophilic inflammation, in chronic rhinosinusitis. However, the mechanism underlying autophagy-mediated regulation of eosinophilic airway inflammation remains unclear. The aim of this review is to provide a general overview of the role of autophagy in eosinophilic airway inflammation. We also suggest that autophagy may be a new therapeutic target for airway inflammation, including that mediated by eosinophils.

• Tuberculosis and Respiratory Diseases
• /
• v.64 no.2
• /
• pp.125-132
• /
• 2008

Background: In chronic obstructive pulmonary disease (COPD) patients, the serum levels of C-reactive protein (CRP) are elevated and an increase of CRP is more exaggerated in the acute exacerbation form of COPD (AECOPD) than in stable COPD. Pulmonary arterial hypertension is a common complication of COPD. An increased level of CRP is known to be associated with the risk of systemic cardio-vascular disorders. However, few findings are available on the potential role of CRP in pulmonary arterial hypertension due to COPD. Methods: This study was performed prospectively and the study population was composed of 72 patients that were hospitalized due to AECOPD. After receiving acute management for AECOPD, serum CRP levels were evaluated, arterial oxygen pressure ($PaO_2$), was measured, and the existence of pulmonary arterial hypertension under room air inhalation was determined in the patients. Results: The number of patients with pulmonary arterial hypertension was 47 (65.3%)., There was an increased prevalence of pulmonary arterial hypertension and an increase of serum CRP levels in patients with the higher stages of COPD (e.g., patients with stage 3 and stage 4 disease; P<0.05). The mean serum CRP levels of patients with pulmonary arterial hypertension and without pulmonary arterial hypertension were $37.6{\pm}7.4mg/L$ and $19.9{\pm}6.6mg/L$, respectively (P<0.05). However, there was no significant difference of the mean values of $PaO_2$ between patients with pulmonary arterial hypertension and without pulmonary arterial hypertension statistically ($77.8{\pm}3.6mmHg$ versus $87.2{\pm}6.0mmHg). Conclusion: We conclude that higher serum levels of CRP can be a sign for pulmonary arterial hypertension in AECOPD patients.

• Journal of Life Science
• /
• v.17 no.2 s.82
• /
• pp.248-253
• /
• 2007

This research investigated whether exposure of diesel exhaust particulate (DEP) and particulate matter (PM) effects on airway remodeling in asthma induced Balb/c and IL-10 knock out (KO) mouse. Mice were sensitized with intraperitoneal injection with ovalbumin, followed by challenges with intranasal ovalbumin. After that mice placed in inhalation chamber and exposed to DEP and $PM(10\;mg/m^3)$. The evidence of airway remodeling was assessed by masson's trichrome staining and PAS staining. The stainability of masson's trichrome and PAS reaction were increased in asthma-induced Baltic mice groups compared with control mice groups. More intensive stainability for masson's trichrome and PAS were appeared in the asthma-induced DEP and PM-exposed groups than asthama-induced groups. But, not significantly increased subepithelial fibrosis and the nember of goblet cell hyperplasia in asthma-induced IL-10 KO mice groups and asthma-induced+DEP and PM-exposed IL-10 KO mice than IL-10 KO mice groups. These results indirectly suggesting that exposure to DEP and PM in asthmatic patients might be aggravate clinical symptoms and IL-10 which seems to play a central role in allergic asthma. In conclusion, DEP and PM exposure might have additive effects on the ovalbumin- induced asthma in a murine model.

• Tuberculosis and Respiratory Diseases
• /
• v.54 no.2
• /
• pp.191-198
• /
• 2003

Background : The pathological features in asthmatic airway remodeling are diverse. The aim of this study was to examine the degree of airway vascularity in relation to the other remodeling parameters in asthmatics. Methods : Bronchial biopsies were done in 34 asthmatic patients, and 6 control subjects. The basement membrane thickness and the subepithelial thickness were measured in the hematoxylin-eosin stained tissue, and the degree of vascularity was measured using type IV collagen immunostaining. Results : 1) Compared to the control subjects, the asthmatics showed a significant increase in the basement membrane thickness ($6.92{\pm}2.01{\mu}m$ vs $9.67{\pm}2.84{\mu}m$, p<0.05) and the subepithelial thickness ($44.49{\pm}31.92{\mu}m$ vs $121.22{\pm}72.79{\mu}m$, p<0.05). 2) Compared to the control subjects, the asthmatics showed a significant increase in the vascular area per unit submucosal area ($4.51{\pm}2.13%$ vs $10.32{\pm}6.08%$, p<0.05). In addition, the number of vessels per unit submucosal area showed an increased tendency without statistical significance. 3) In the asthmatics, the number of vessels and the vascular area per unit submucosal area showed no correlation with the basement membrane thickness, the subepithelial thickness, the severity, the forced expiratory volume in 1 second($FEV_1$), and the methacholine provocative concentration 20($PC_{20}$). Conclusion : This study showed that vascularity was an important parameter in asthmatic airway remodeling but it was not related to the other remodeling parameters such as the basement membrane thickness and the subepithelial thickness. Each of these asthmatic remodeling parameters may have a different clinical significance. Therefore, further studies will be needed.

• IMMUNE NETWORK
• /
• v.21 no.3
• /
• pp.19.1-19.18
• /
• 2021

Clinical and molecular phenotypes of asthma are complex. The main phenotypes of adult asthma are characterized by eosinophil and/or neutrophil cell dominant airway inflammation that represent distinct clinical features. Upper and lower airways constitute a unique system and their interaction shows functional complementarity. Although human upper airway contains various indigenous commensals and opportunistic pathogenic microbiome, imbalance of this interactions lead to pathogen overgrowth and increased inflammation and airway remodeling. Competition for epithelial cell attachment, different susceptibilities to host defense molecules and antimicrobial peptides, and the production of proinflammatory cytokine and pattern recognition receptors possibly determine the pattern of this inflammation. Exposure to environmental factors, including infection, air pollution, smoking is commonly associated with asthma comorbidity, severity, exacerbation and resistance to anti-microbial and steroid treatment, and these effects may also be modulated by host and microbial genetics. Administration of probiotic, antibiotic and corticosteroid treatment for asthma may modify the composition of resident microbiota and clinical features. This review summarizes the effect of some environmental factors on the upper respiratory microbiome, the interaction between host-microbiome, and potential impact of asthma treatment on the composition of the upper airway microbiome.

• Tuberculosis and Respiratory Diseases
• /
• v.71 no.3
• /
• pp.172-179
• /
• 2011

Background: Statins can regulate the production of pro-inflammatory cytokines and inhibit MMP production or activation in a variety of types of cells. This study evaluated whether statins would inhibit MMP release from human lung fibroblasts, which play a major role in remodeling processes. Methods: This study, using an in-vitro model (three-dimensional collagen gel contraction system), evaluated the effect of cytokines (tumor necrosis factor-${\alpha}$, TNF-a and interleukin-$1{\beta}$, IL-1b) on the MMP release and MMP activation from human lung fibroblasts. Collagen degradation induced by cytokines and neutrophil elastase (NE) was evaluated by quantifying hydroxyproline. Results: In three-dimensional collagen gel cultures (3D cultures) where cytokines (TNF-a and IL-1b) can induce the production of MMPs by fibroblasts, it was found that simvastatin inhibited MMP release. In 3D cultures, cytokines together with NE induced collagen degradation and can lead to activation of the MMP, which was inhibited by simvastatin. Conclusion: Simvastatin may play a role in regulating human lung fibroblast functions in repair and remodeling processes by inhibiting MMP release and the conversion from the latent to the active form of MMP.

• The Journal of Internal Korean Medicine
• /
• v.39 no.4
• /
• pp.451-462
• /
• 2018

Hubakmawhang-tang (HMT), listed in Geumgweyoryak, is an oriental medicine used for the symptoms of asthma, such as cough and dyspnea. In this study, we investigated the HMT effects on ovalbumin-induced asthmatic in mice. We examined weight changes, airway hyperresponsiveness, histopathological abnormalities, immune cell infiltrations, immunoglobulin and inflammatory cytokine levels, and spleen body weight ratios in asthmatic mice. HMT inhibited airway hyperresponsiveness, immune cell infiltration, and airway remodeling and caused a significant lowering of serum IgE and IgG1 levels. The asthmatic mice had elevated IL-4 levels in lung tissue and this elevation was effectively prevented by HMT. HMT did not cause changes in body weight or in the spleen body weight ratio. Therefore, HMT might have an anti-asthmatic effect in the ovalbumin-induced mouse model.

• The Journal of Internal Korean Medicine
• /
• v.25 no.4
• /
• pp.260-273
• /
• 2004

Backgrounds : In recent years, asthma has become recognized as a chronic inflammatory disease associated pathologically with airway epithelial inflammation and airway remodeling. Objectives : To evaluate the different effects of Hirudo depending upon pharmaceutical manufactures on the expression and the activities of IL-6 and GM-CSF in airway epithelial cells, samples of Hirudo(水蛭), Hirudo toasted with Talcum(水蛭滑石炒) and Hirudo toasted with Ephedrae Herba(水蛭麻黃炒) were tested. Methods : After inducing enhanced messenger RNA(mRNA) expression and secretion of each cytokine by tumor necrosis factor-alpha(10 ng/ml) treatment, cultured human bronchial epithelial cell line BEAS-2B was added to each sample$(l,\;10,\;100\;&\;1000\;{\mu}g/ml)$. Subsequently, DNA activities were analyzed. Specifically mRNA expression and culture supernatants(protein levels) of IL-6 and GM-CSF from BEAS-2B cells, were analyzed using luciferase reporter gene assay, reverse transcription-polymerase chain reaction(RT-PCR) analysis and enzyme-linked immunosorbent assay. Results : Hirudo toasted with Ephedrae Herba(水蛭麻黃炒) and Hirudo(水蛭) inhibited IL-6 activities in BEAS-2B cells remarkably, and inhibited mRNA expression levels and protein levels in supernatant of IL-6 and GM-CSF at various concentrations, significantly(p<0.05). However, Hirudo toasted with Talcum(水蛭滑石炒) had no effect on mRNA expression levels and showed a slight inhibitory effect on GM-CSF protein levels in supernatant of culture medium. Conclusions : These results strongly suggest that Hirudo toasted with Ephedrae Herba(水蛭麻黃炒) and Hirudo(水蛭) would be serve as effective medicaments in the treatment of airway inflammation and remodeling of asthmatic patients.