• IMMUNE NETWORK
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• 제19권1호
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• pp.5.1-5.12
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• 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.

• 대한본초학회지
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• 제26권4호
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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.

• Tuberculosis and Respiratory Diseases
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• 제80권4호
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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.

• 대한후두음성언어의학회지
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• 제27권2호
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• pp.87-90
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• 2016

Cough, the most common symptom, encountered in the outpatient clinic can be caused by various underlying diseases. It defines as chronic cough that the duration of cough is more than 8 weeks with a normal chest X-ray findings. The cause of cough can be found out for more than 90% through the appropriate diagnostic approach and Upper airway cough syndrome, Asthma and Gastroesophageal reflex disease are the most common causes of disease to non-smokers. Chronic cough can be due to not one reason but various reasons and achieve good results by a systematic approach to diagnosis and a concrete treatment on the basis of the sufficient understanding of the underlying disease.

• Biomolecules & Therapeutics
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• 제8권2호
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• pp.107-112
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• 2000

To investigate the alteration of airway mucin in airway disease patients, immunoassay procedures were employed using monoclonal antibodies HM02 and HM03 (Hybridoma, 18,457-463, 1999). Alteration of mucin release was determined by ELISA and the integrity of mucin was determined by Western blot. In ELISA, it was found that mucin release increased from pneumonia, chronic cough, bronchiectasis, eosinophilic pneumonia, lung cancer and bronchial asthma patients. In Western blot, the increase in immunoreactivity was observed in case of pneumonia, chronic cough, bronchiectasis and bronchial asthma. In bronchial asthma, there was no obvious degradation of mucin while in other diseases, varying degree of mucin degradation was observed. The data from the present study implicate that HMO2 and HM03 are suitable for the immunological analysis of mucin in airway disease patients. The role of increased mucin release and varying degree of mucin degradation on airway diseases should be further investigated in the future.

• IMMUNE NETWORK
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• 제22권6호
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• pp.45.1-45.15
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• 2022

Asthma is a chronic airway inflammatory disease characterized by reversible airway obstruction and airway hyperreactivity to various environmental stimuli, leading to recurrent cough, dyspnea, and wheezing episodes. Regarding inflammatory mechanisms, type 2/eosinophilic inflammation along with activated mast cells is the major one; however, diverse mechanisms, including structural cells-derived and non-type 2/neutrophilic inflammations are involved, presenting heterogenous phenotypes. Although most asthmatic patients could be properly controlled by the guided treatment, patients with severe asthma (SA; classified as a treatment-refractory group) suffer from uncontrolled symptoms with frequent asthma exacerbations even on regular anti-inflammatory medications, raising needs for additional controllers, including biologics that target specific molecules found in asthmatic airway, and achieving the precision medicine for asthma. This review summarizes the immunologic basis of airway inflammatory mechanisms and current biologics for SA in order to address unmet needs for future targets.

• Tuberculosis and Respiratory Diseases
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• 제73권2호
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• pp.122-126
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• 2012

Plastic bronchitis is a rare disease characterized by marked airway obstruction, via the formation of large gelatinous or rigid airway cast. In Korea, there were a few case reports with plastic bronchitis not in adults, but in children. So we report a case of an adult who was diagnosed as plastic bronchitis with eosinophilic casts, with no history of atopic and cardiac disease.

• Tuberculosis and Respiratory Diseases
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• 제77권6호
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• pp.237-242
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• 2014

Asthma is a chronic inflammatory disease of the airway that comprises a variety of etiologies and inflammatory phenotypes. Clinically, there is a wide range of patients with varying severities and responses to individual drugs. The introduction of inhaled corticosteroid therapy has dramatically changed the treatment of asthma. Recent development of new therapies suggests the possibility of another breakthrough. These can be categorized as follows: anti-cytokine therapies that usually target eosinophilic inflammation, sublingual immunotherapy, and bronchial thermoplasty. In this paper, we will review the major articles related to asthma treatment that were published in 2013.

• Clinical and Experimental Pediatrics
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• 제52권9호
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• pp.1048-1052
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• 2009

증식성 기관지염(plastic bronchitis)은 드문 질환으로 일반적인 점액전에 비해 크고 접착력이 있는 가지모양의 점액성 기관지 주형(cast)을 반복적으로 형성한다. 이 주형은 크기가 다양하여 자연적으로 배출되기도 하나 제거를 위해 기관지경이 필요하기도 한다. 따라서 증식성 기관지염에서 큰 기도의 폐쇄가 발생하면 생명을 위협할 수 있다. 호산구성 주형을 가진 보고된 환자 22명 중 3명이 중심 기도 폐쇄로 인해 사망에 이르렀다. 본 저자들은 아토피나 알레르기, 선천성 심장병의 병력이 없는 건강했던 소아에서 호산구성 증식성 기관지염을 진단하여 보고한다. 항생제와 스테로이드의 정주와 물리 치료를 포함한 적극적인 폐 청소와 주기적인 주형의 기관지경 제거를 시행하였으나 저산소성 뇌 손상에 이어 뇌사에 이르렀다. 본 증례와 같이 증식성 기관지염이 중심 기도를 막았을 때 생명을 위협할 수 있다. 따라서 증식성 기관지염의 증상이나 징후가 보일 경우 조기 치료가 필요하리라 생각된다.

• Tuberculosis and Respiratory Diseases
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• 제83권3호
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• pp.185-194
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• 2020

Blood eosinophil counts have emerged as a chronic obstructive pulmonary disease (COPD) biomarker that predict the effects of inhaled corticosteroids (ICS) in clinical practice. Post-hoc and prospective analysis of randomized control trials have shown that higher blood eosinophil counts at the start of the study predict a greater response to ICS. COPD patients with frequent exacerbations (2 or more moderate exacerbations/yr) or a history of hospitalization have a greater response to ICS. Ex-smokers also appear to have a greater ICS response. Blood eosinophil counts can be combined with clinical information such as exacerbation history and smoking status to enable a precision medicine approach to the use of ICS. Higher blood eosinophil counts are associated with increased eosinophilic lung inflammation, and other biological features that may contribute to the increased ICS response observed. Emerging data indicates that lower blood eosinophil counts are associated with an increased risk of bacterial infection, suggesting complex relationships between eosinophils, ICS response, and the airway microbiome.