• Journal of Yeungnam Medical Science
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• v.36 no.1
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• pp.8-15
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• 2019

Connective tissue diseases (CTDs) can affect all compartments of the lungs, including airways, alveoli, interstitium, vessels, and pleura. CTD-associated lung diseases (CTD-LDs) may present as diffuse lung disease or as focal lesions, and there is significant heterogeneity between the individual CTDs in their clinical and pathological manifestations. CTD-LDs may presage the clinical diagnosis a primary CTD, or it may develop in the context of an established CTD diagnosis. CTD-LDs reveal acute, chronic or mixed pattern of lung and pleural manifestations. Histopathological findings of diverse morphological changes can be present in CTD-LDs airway lesions (chronic bronchitis/bronchiolitis, follicular bronchiolitis, etc.), interstitial lung diseases (nonspecific interstitial pneumonia/fibrosis, usual interstitial pneumonia, lymphocytic interstitial pneumonia, diffuse alveolar damage, and organizing pneumonia), pleural changes (acute fibrinous or chronic fibrous pleuritis), and vascular changes (vasculitis, capillaritis, pulmonary hemorrhage, etc.). CTD patients can be exposed to various infectious diseases when taking immunosuppressive drugs. Histopathological patterns of CTD-LDs are generally nonspecific, and other diseases that can cause similar lesions in the lungs must be considered before the diagnosis of CTD-LDs. A multidisciplinary team involving pathologists, clinicians, and radiologists can adequately make a proper diagnosis of CTD-LDs.

• 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 Journal of Korean Medicine
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• v.39 no.4
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• pp.126-135
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• 2018

Objectives: Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation and irreversible airflow. This study aimed to evaluate the effects of GHX02 in a COPD-induced mouse model. Methods: The COPD mouse model was established by exposure to cigarette smoke extract and lipopolysaccharide which were administered by intratracheal injection three times with a 7 day interval. GHX02 (100, 200, 400 mg/kg) and all other drugs were orally administrated for 14 days from Day 7 to Day 21. Results: GHX02 significantly decreased the neutrophil counts in bronchoalveolar lavage fluid (BALF) and the number of $CD4^+$, $CD8^+$, $CD69^+$, and $CD11b^+/GR1^+$ cells in BALF and lung cells. GHX02 also suppressed the secretion of tumor necrosis factor-alpha ($TNF-{\alpha}$), interleukin-17A, macrophage inflammatory protein 2 (MIP2), and chemokine (C-X-C motif) ligand 1 (CXCL-1) in BALF and ameliorated the lung pathological changes. Conclusions: Thus, GHX02 effectively inhibited airway inflammation by inhibiting migration of inflammatory cells and expression of pro-inflammatory cytokines. Therefore, GHX02 may be a promising therapeutic agent for COPD.

• Korean Journal of Radiology
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• v.24 no.8
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• pp.795-806
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• 2023

Occupational lung diseases (OLD) are a group of preventable conditions caused by noxious inhalation exposure in the workplace. Workers in various industries are at a higher risk of developing OLD. Despite regulations contributing to a decreased incidence, OLD remain among the most frequently diagnosed work-related conditions, contributing to significant morbidity and mortality. A multidisciplinary discussion (MDD) is necessary for a timely diagnosis. Imaging, particularly computed tomography, plays a central role in diagnosing OLD and excluding other inhalational lung diseases. OLD can be broadly classified into fibrotic and non-fibrotic forms. Imaging reflects variable degrees of inflammation and fibrosis involving the airways, parenchyma, and pleura. Common manifestations include classical pneumoconioses, chronic granulomatous diseases (CGD), and small and large airway diseases. Imaging is influenced by the type of inciting exposure. The findings of airway disease may be subtle or solely uncovered upon expiration. High-resolution chest CT, including expiratory-phase imaging, should be performed in all patients with suspected OLD. Radiologists should familiarize themselves with these imaging features to improve diagnostic accuracy.

• Tuberculosis and Respiratory Diseases
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• v.83 no.3
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• pp.175-184
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• 2020

Quantitative sputum cytometry facilitates in assessing the nature of bronchitis associated with exacerbations of chronic obstructive pulmonary disease (COPD). This is not assessed in most clinical trials that evaluate the effectiveness of strategies to prevent or to treat exacerbations. While up to a quarter of exacerbations may be associated with raised eosinophil numbers, the vast majority of exacerbations are associated with neutrophilic bronchitis that may indicate airway infections. While eosinophilia may be a predictor of response to corticosteroids (oral and inhaled), the limited efficacy of anti-interleukin 5 therapies would suggest that eosinophils may not directly contribute to those exacerbations. However, they may contribute to airspace enlargement in patients with COPD through various mechanisms involving the interleukin 13 and matrix metalloprotease pathways. The absence of eosinophils may facilitate in limiting the unnecessary use of corticosteroids. The presence of neutrophiia could prompt an investigation for the specific pathogens in the airway. Additionally, sputum measurements may also provide insight into the mechanisms of susceptibility to airway infections. Iron within sputum macrophages, identified by hemosiderin staining (and by more direct quantification) may impair macrophage functions while the low levels of immunoglobulins in sputum may also contribute to airway infections. The assessment of sputum at the time of exacerbations thus would facilitate in customizing treatment and treat current exacerbations and reduce future risk of exacerbations.

• Tuberculosis and Respiratory Diseases
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• v.49 no.1
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• pp.82-92
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• 2000

Background : In chronic airway disease, mucus secretion is increased, but extraction of mucin, which is the main component of mucus secretion, is a very complicated and limited in clinical use. Recently, monoclonal antibody for mucin was developed for possible clinical use. In this study, cellular analysis and quantification of respiratory mucin in sputum of patients with chronic airway diseases were performed. Method : Sputum was collected from patients with asthma(n=33), bronchiectasis(n=8) or chronic bronchitis (n=13) by spontaneous expectoration or by hypertonic saline induction. Collected sputums was treated by 0.1% dithiotreitol to dissociate the disulfide bond of the mucus and filtered through a nylon gauze. Total cell count, viability and differential count were measured. For detection of mucin, collected samples were treated with sodium dodecyl sulfate polyacrylamide gel electrophoresis and then with monoclonal antibody(HMO2), as the primary antibody, and PAS stain. The amount of mucin was measured with ELISA by HMO2. Correlation with clinical information, cellular analysis, and amount of measured mucin were analyzed. Results : Total cell counts of sputum were significantly increased in patients with bronchiectasis but viability remained the same. Eosinophils were significantly increased in patients with asthma, neutrophils in bronchiectasis chronic bronchitis, respectively (p<0.05). The results of Western blotting and PAS staining confirmed the presence of glycoproteins and matched? with mucin. The amounts of mucin measured by ELISA were not significantly different among the disease groups. Significant correlation was identified between the amount of mucin and viability(r=-0.482, p<0.05). Conclusion : Inflammatory cells in the sputum of those with chronic airway disease were different for each disease type. Measurement of mucin by ELISA via monoclonal antibodies may be a simple method for the evaluation of chronic airway disease.

• IMMUNE NETWORK
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• v.14 no.5
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• pp.249-254
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• 2014

Allergic asthma is a chronic pulmonary inflammatory disease characterized by reversible airway obstruction, hyperresponsiveness and eosinophils infiltration. Toll-like receptors (TLRs) signaling are closely associated with asthma and have emerged as a novel therapeutic target in allergic disease. The functions of TLR3 and TLR4 in allergic airway inflammation have been studied; however, the precise role of TIR-domain-containing adapter-inducing interferon-${\beta}$ (TRIF), the adaptor molecule for both TLR3 and TLR4, is not yet fully understood. To investigate this, we developed a mouse model of OVA-induced allergic airway inflammation and compared the severity of allergic airway inflammation in WT and $TRIF^-/^-$ mice. Histopathological assessment revealed that the severity of inflammation in airway inflammation in TRIF-deficient mice was comparable to that in WT mice. The total number of cells recovered from bronchoalveolar lavage fluid did not differ between WT and TRIF-deficient mice. Moreover, TRIF deficiency did not affect Th1 and Th2 cytokine production in lung tissue nor the level of serum OVA-specific IgE, $IgG_1$ and $IgG_{2c}$. These findings suggest that TRIF-mediated signaling may not be critical for the development of allergic airway inflammation.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.2
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• pp.157-163
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• 2020

Chronic inflammatory airway diseases, such as chronic rhinosinusitis, chronic obstructive pulmonary disease, and asthma, are associated with excessive mucus production. Hence, the regulation of mucus production is important for the treatment of upper and lower airway diseases. Eupatilin is a pharmacologically active ingredient obtained from Artemisia asiatica Nakai (Asteraceae) and exerts potent anti-inflammatory, anti-allergic, and anti-tumor activities. In the present study, we investigated the effect of eupatilin on phorbol 12-myristate 13-acetate (PMA)-induced MUC5AC and MUC5B expression in human airway epithelial cells. We found that eupatilin treatment significantly inhibited PMA-induced mucus secretion in PAS staining. In addition, qRT-PCR results showed that eupatilin dose-dependently decreased the mRNA expression of MUC5AC in human airway epithelial cells. Western blot and immunofluorescence assay also showed that PMA-induced protein expression of MUC5AC was inhibited by eupatilin treatment. Finally, we investigated MAPKs activity after stimulation with PMA using western blot analysis in human airway epithelial cells. The results showed that eupatilin downregulated the levels of phosphorylated p38, ERK, and JNK. In summary, the anti-inflammatory activities of eupatilin, characterized as the suppression of MUC5AC expression and secretion in human airway epithelial cells, were found to be associated with the inhibition of p38/ERK/JNK MAPKs signaling pathway of MUC5AC secretion.

• Tuberculosis and Respiratory Diseases
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• v.47 no.6
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• pp.786-796
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• 1999

Background: It has been anticipated that the amount and composition of mucin are changed in patients with chronic airway diseases. We evaluated whether RTO3(mAb against rat tracheal mucins) could quantify the amount of mucin from the airway in the patients with chronic airway diseases. Methods and results; 1) RTO3 was bound to high molecular weight of mucin based on Western blot in sputum and BALF from patients with chronic airway diseases. 2) The goblet cells and submucosal glands in main bronchus from human were observed by PAS stain. And immunohistochemical stain with RTO3 showed immunoreactivity on some goblet cells. 3) The amount of mucin was more increased in patients with chronic airway diseases compared to those in normal subjects. 4) In the exacerbation of asthmatics, mucin amounts were more increased than stable asthmatics. Conclusion: We suggested that secreted mucin in chronic airway diseases can be quantified by ELISA with RTO3.

• 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.