• Parasites, Hosts and Diseases
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• v.62 no.3
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• pp.365-377
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• 2024

Exposure to storage mite (SM) and house dust mite (HDM) allergens is a risk factor for sensitization and asthma development; however, the related immune responses and their pathology have not been fully investigated. The HDMs Dermatophagoides farinae and Dermatophagoides pteronyssinus and SM Tyrophagus putrescentiae are potent allergens that induce asthma. Most SM-related studies have focused on the allergic reactions of individuals by measuring their immunoglobulin (Ig)E expression. Considering the limited research on this topic, the present study aims to investigate the differences in the immune responses induced by HDMs and SMs and histologically analyze lung tissues in a mouse asthma model to understand the differential effects of HDM and SM. The results revealed that all mite species induced airway inflammation. Mice challenged with T. putrescentiae had the highest airway resistance and total cell, eosinophil, and neutrophil counts in the bronchoalveolar lavage fluid (BALF). The SM-sensitized groups showed more severe lesions and mucus hypersecretions than the HDM-sensitized groups. Although the degree of HDM and SM exposure was the same, the damage to the respiratory lung tissue was more severe in SM-exposed mice, which resulted in excessive mucin secretion and increased fibrosis. Furthermore, these findings suggest that SM sensitization induces a more significant hypersensitivity response in mucosal immunity than HDM sensitization in asthma models.

• Tuberculosis and Respiratory Diseases
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• v.43 no.4
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• pp.547-557
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• 1996

Background : An excessive accumulation of neutrophils in lung tissue has been known to play an important role in mediating the tissue injury among the adult respiratory distress syndrome, idiopathic pulmonary fibrosis and cystic fibrosis by releasing toxic oxygen radicals and proteolytic enzymes. Therefore, it is important to understand a possible mechanism of neutrophil accumulation in lung tissue. In many species, exposure to hyperoxic stimuli can cause changes of lung tissues very similar to human adult respiratory distress syndrome and neutrophils are also functioning as the main effector cells in hyperoxic lung injury. The purpose of the present study was to examine whether neutrophils function as a key effector cell and to study the nature of possible neutrophil chemotactic factors found in bronchoalveolar lavage fluid from the hyperoxia exposed rats. Methods : We exposed the rats to the more than 95% oxygen for 24, 48, 60 arid 72 hours and bronchoalveolar lavage(BAL) was performed. Neutrophil chemotactic activity was measured from the BAT- fluid of each experimental groups. We also evaluated the molecular weight of neutrophil chemotactic tractors using fast performance liquid chromatography and characterized the substances by dialyzer membrane and heat treatment. Results : 1) The neutrophil proportions in bronchoalveolar lavage fluid began to rise from 48 hours after oxygen exposure, and continued to be significantly increased with exposure times. 2) chemotactic index for neutrophils in lung lavages from rats exposed to hyperoxia was significantly higher in 48 hours group than in control group, and was significantly increased with exposure time. 3) No deaths occured until after 48 hours of exposure. However, mortality rates were increased to 33.3 % in 60 hours group and 81.3 % in 72 fours group. 4) Gel filtration using fast performance liquid chromatography disclosed two peaks of neutrophil chemotactic activity in molecular weight of 104,000 and 12,000 daltons. 5) Chemotactic indices of bronchoalveolar lavage fluid were significantly deceased when bronchoalveolar lavage fluid was treated with heat ($56^{\circ}C$ for 30 min or $100^{\circ}C$ for 10 min) or dialyzed (dialyzer membrane molecular weight cut off : 12,000 daltons). Conclusion : These results suggested that the generation of neutrophil chemotactic factor and subsequent neutrophil influx into the lungs are playing an important roles in hyperoxia-induced acute lung injury. Neutrophil chemotactic factor in the lung lavage fluids consisted of several distinct components having different molecular weight and different physical characteristics.

• Tuberculosis and Respiratory Diseases
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• v.66 no.2
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• pp.141-151
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• 2009

Background: There is limited data on the epidemiology and relative frequency of idiopathic interstitial pneumonia (IIP) worldwide. This survey was performed to assess the epidemiology and relative frequency of IIP in Korea. Methods: The patients with IIP and who were confirmed by lung biopsy, except those patients with idiopathic pulmonary fibrosis, (IPF) over a 5 year period (from Jan. $1^{st}$, 2003 to Dec. $31^{st}$, 2007) were registered by a web-base questionnaire. Results: A total of 3,156 cases were registered, but 970 cases were excluded due to duplicative registration, inadequate data and the unmet ATS/ERS diagnostic criteria. A total of 2,186 cases were analyzed. The male to female ratio was about 2 : 1 and their mean age was 65 (range: 11-94). The most frequent disease was IPF (77.1%), followed in decreasing order by nonspecific interstitial pneumonia (NSIP) (11.9%), cryptogenic organizing pneumonia (COP) (8.5%), acute interstitial pneumonia (AIP) (1.1%), desquamative interstitial pneumonia (DIP) (0.9%), respiratory bronchiolitis-interstitial lung disease (RB-ILD) (0.4%) and lymphocytic interstitial pneumonia (LIP) (0.1%). The mean age of the patients with IPF, NSIP and COP was 67.8, 57.1 and 57.7 years old, respectively. The most frequent symptom was dyspnea on exertion (69%) followed by coughing (61%) and sputum (33%) for the whole population. The three year survival rate was 62% for the patients with IPF and the five year survival rate was 85% in both the NSIP and COP patients. Conclusion: This survey provides helpful information for the management of IIP and to produce management guidelines for this illness in Korea.

• Journal of Oral Medicine and Pain
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• v.8 no.1
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• pp.83-96
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• 1983

The purpose of this study was detection of the poison from the acute cyanide and aresenic poisoned rabbits, The author administered KCN and $AS_2O_3$ to rabbits and caused acute poisoning, then analysed the teeth, dental pulp and jaws of the rabbits chemicotoxicologically and observed the specimen histopathologically. 1. In subcutaneausly injected group of KCN, a large amount of cyanide was detected in blood and lung and a small amount of cyanide was detected in teeth and dental pulp, but was not detected in jaws. 2. In orally administered group of KCN a large amount of cyanide was detected in blood, lung and dental pulp and a small amount of cyanide was detected in teeth and jaws. 3. In orally administered group of $AS_2O_3$, arsenic was detected markedly in teeth and jaws, but was detected a little in dental pulp. 4. In orally administered and heat-treated group of KCN, the author could detected cyanide in teeth, dental pulp and jaws. 5. In suvcutanelusly injected group of KCN, orally administered group of KCN and orally dministered group of $AS_2O_3$, histopathologic findings showed the congestion and hemorrhage in dental pulp. 6. In orally administerd group of $AS_2O_3$, the congestion and hemorrhage in buccal mucosa were found and the basal cell degeneration and fibrosis were found in palatal mucosa.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.7
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• pp.3405-3409
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• 2016

Malignant pleural mesothelioma (MPM), an aggressive malignant tumor of mesothelial origin associated with asbestos exposure, shows a limited response to conventional chemotherapy and radiotherapy. Therefore, the overall survival of MPM patients remains very poor. Progress in the development of therapeutic strategies for MPM has been limited. We recently reported that the calpain inhibitor, calpeptin exerted inhibitory effects on pulmonary fibrosis by inhibiting the proliferation of lung fibroblasts. In the present study, we examined the preventive effects of calpeptin on the cell growth of MPM, the origin of which is mesenchymal cells, similar to lung fibroblasts. Calpeptin inhibited the proliferation of MPM cells, but not mesothelial cells. It also prevented 1) the expression of angiopoietin (Ang)-1 and Tie-2 mRNA in MPM cells, but not mesothelial cells and 2) the Ang-1-induced proliferation of MPM cells through an NF-kB dependent pathway, which may be the mechanism underlying the preventive effects of calpeptin on the growth of MPM cells. These results suggest potential clinical use of calpeptin for the treatment of MPM.

• Journal of Chest Surgery
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• v.39 no.3 s.260
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• pp.248-250
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• 2006

A 48-years-old woman was visited to our hospital because of incidental finding of intrapulmonary foreign body. Chest X-ray showed a 4cm sized foreign body in left upper lung field without adjacent fibrosis. Chest CT showed a sewing needle shaped foreign body of metallic density, located in the 113ft upper lobe. The foreign bodies including the needle were removed surgically using a wedge resection. The extracted needle was divided into three 4 cm pieces. Patient was discharged without other respiratory symptoms after surgery. We report a case of wedge resection in a patient with intrapulmonary needle in the left upper lobe, with review of literatures.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.125-125
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• 2003

Respiratory effects in full time welders include bronchitis, airway irritation, lung function changes, and lung fibrosis. Welder's pneumoconiosis has been generally determined to be benign and not associated with respiratory symptoms based on the absence of pulmonary function abnormalities in welders with marked radiographic abnormalities.(omitted)

• Tuberculosis and Respiratory Diseases
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• v.51 no.6
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• pp.597-602
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• 2001

A 47-years-old woman presented with a 2-month history of a dry mouth and dry cough. The patient had been taking medication for Sj$\ddot{o}$gren's syndrome for approximately 7 years. The chest radiography showed multiple cystic lesions and a hazy density in both lower lung fields. The HRCT showed a diffuse ground glass like appearance and multiple variable sized cystic lesions in both lung fields. After medication, the symptoms were aggravated. Bronchoscopy was preformed with a transbronchial lung biopsy. The biopsies showed an infiltration of lymphocytes, neutrophils, monocytes and histiocytes through the interstitial space of the alveola and a widening of the alveolar septa. However, the histological findings of the cysts were not obtained. Sj$\ddot{o}$gren's syndrome is a slowly progressive inflammatory autoimmune disease, which is characterized by lymphocyte mediated destruction of the exocrine glands, with pulmonary involvement in approximately 19-65%, High-resolution CT is a sensitive technique for assessing the pulmonary involvement in patients with Sj$\ddot{o}$gren's syndrome. Although a lung biopsy is not always necessary for establishing a diagnosis of an interstitial lung disease in Sj$\ddot{o}$gren's syndrome. A lung biopsy may reveal a wide spectrum of changes ranging from a mild inflammatory response to end stage fibrosis with honeycombing. Because of the predominantly peribronchiolar inflammatory infiltration and inspissated secretions the cysts were suspected to have been formed by the ball-valve phenomen. However, no definite evidence was obtained.

• Radiation Oncology Journal
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• v.19 no.2
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• pp.181-189
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• 2001

Purpose : Changes in the balance between MMP and TIMP can have a profound effect on the composition in the extracellular matrix (ECM) and affect various cellular functions including adhesion, migration, differentiation of cells, and fibrosis and invasion and metastasis of cancer cells. Radiation therapy is a popular treatment modality for benign and malignant tumor, but the study for radiation effect on MMP and TIMP is scarce. In the current study, we have examined the expression of TIMP in fibrosis-prone (C57BL/6) mice after radiation. Methods and Materials : Adult female mice of $10\~12$ weeks were used. The whole body were irradiated using a Varian CL-4/100 with 2 and 10 Gy. Immunohistochemical staining was peformed according to Avidin Biotin complex method and evaluated by observing high power field. For TIMP-1, TIMP-2 antibodies, reactivity was assessed in the parenchymal cell and in the stromal cell. The scale of staining was assessed by combining the quantitative and qualiative intensity of staining. Results : TIMP-1 immunoreactivity did not change in lung. But, in liver, TIMP-1 immunoreactivity was localized in cytoplasm of hepatocyte and Kupffer cell. in kidney, TIMP-1 immunoreactivity was localized in cytoplasm of some tubular cell. Temporal variations were not seen. Dose-response relationship was not seen except kidney. TIMP-2 immunoreactivity in lung was a score (++) at 0 Gy and elevated to a score (+++) at 2 Gy. TIMP-2 immunoreactivity was a score (++) in liver at 0 Gy. TIMP-2 immunoreactivity was localized in cytoplasm of hepatocyte and Kupffer cell as same as patterns of TIMP-1 immunoreactivity. The TIMP-2 immunoreactivity in liver was elevated to (+++) at 2 Gy. Immunoreactivity to TIMP-2 in kidney was a score (+++) at 0 Gy and was not changed at 10 Gy. The score of TIMP-2 immunoreactivity was reduced to (++) at 2 Gy. TIMP-2 immunoreactivity was confined to tubules in kidney. Temporal variation of TIMP-2 immunoreactivity was irregular. Dose-response relationship of TIMP-2 immunoreactivity was not seen. Conclusions : Differences between intensity of expression of TIMP-1 and TIMP-2 in each organ was present. Expression of TIMP was localized to specific cell in each organ. Irradiation increased TIMP-1 immunoreactivity in the liver and the kidney. Irradiation increased TIMP-2 immunoreactivity in the lung. But, in the liver and the kidney, TIMP-2 expression to radiation was irregular. Temporal variation of TIMP-2 immunoreactivity was irregular. Dose-response relationship of TIHP-2 immunoreactivity was not seen. In the future, we expect that the study of immunohistochemical staining of longer period of postirradiation and quantitative analysis using western blotting and northern blotting could define the role of TIMP in the radiation induced tissue fibrosis.

• Radiation Oncology Journal
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• v.17 no.3
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• pp.238-248
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• 1999

Purpose : To assess the histomorphologic changes in the rat lung injury induced by radiation, to determine whether captopril reduces the rat lung injury and to evaluate change in TNF-${\alpha}$ and TGF-${\beta}$ in rat lung damage by radiation and captopril Methods and material : Right lungs in male Sprague-Dawley rats were divided irradiation alone (10, 20, 30 Gy) or radiation (same dose with radiation alone group) with captopril (500 mg/L). Radiation alone group were sacrificed at twelve hours and eleven weeks after radiation and radiation with captopril group (captopril group) were sacrificed at eleven weeks after radiation with captopril. We examined the light microscope and electron microscopic features in the groups. Results : In radiation alone group, there were patch parenchymal collapse and consolidation at twelve hours after radiation. The increase of radiation dose shows more prominent the severity and broader the affected areas. Eleven weeks after radiation, the severity and areas of fibrosis had increased in proportion to radiation dose given in the radiation alone group. There was notable decrease of lung fibrosis in captopril group than in radiation alone group. The number of mast cells rapidly increased with increase of radiation dose in radiation alone group and the degree of increase of mast cell number and severity of collagen accumulation more decreased in captopril group than in radiation alone group. In radiation alone group, expression of TNF-${\alpha}$ and TGF-${\beta}$ increased according to increase of radiation dose at twelve hours after radiation in both group. At eleven weeks after radiation, expression of TGF-${\beta}$ increased according to increase of radiation dose in radiation group but somewhat decreased in captopril group. In the captopril group the collagen deposition increased but less dense than those of radiation alone group. The severity of perivascular thickening, capillary change, the number and degranulation of mast cells more decreased in the captopril group than in the radiation alone group. Conclusion : It is concluded that the effect of captopril in the rat lungs after radiation was considered to be due to its effect on inhibition of mast cells and reduction of collagen deposition, and captopril may be protect in lung damage after radiation. We observed expression of TNF-${\alpha}$ and TGF-${\beta}$ increased at the early phase after radiation and expression of TGF-${\beta}$ increased in proportion to increase of radiation dose at the chronic phase after radiation. This results will contribute to future investigation in reduction mechanism of captopril in lung damage after radiation.