• The Korean Journal of Zoology
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• v.32 no.2
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• pp.107-119
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• 1989

The histochemical characteristics of the cutaneous granular glands and its fine structure of the Korean fire bellied toad, Bombino orientalis Boulenger the only species inhabitated in Korea, were studied with light and electron microscopes. By the granular size and histochemical properties, the granular glands were subdivided into two types. The type I glands have small secretory granules (3.6 $\mu$ m), whereas the type II glands contain relatively larger granules (7.5 $\mu$ m). These two types of glands were simple alveolar gland, and they were commonly composed of inner glandular epithelial cells and outermost myoepithelial cells. By the histochemical reactions, these two secretory granules were not responsed to Alcian blue, but weakly positive reaction was observed in type I granular glands by the PAS reaction. And by the scanning electron microscopic observation, extemal morphology of the opening site of the gland duct was resembled to the stomata of the plant leaves. Especially the epithelial cells of the type I glands had fine reticular surface whereas, type II glands had large vesicular surface. These types of the glands conimonly had larger cavities than those of mucous glands, and forming the multinucleated unicellulr structure (syncytium) at the glandular epithelial layers. Secretory granules of these glands were originated from the rough endoplasmic reticulum of the glandular epithelial cells, and by the maturation level of the granule, morphological diversities appeared.

• Applied Microscopy
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• v.31 no.1
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• pp.71-83
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• 2001

Laminin, a kind of multidomain glycoproteins, is mainly localized in the basement membranes of various tissues. It is known that laminin plays an important part in mammalian lung morphogenesis. The authors have undertaken this study to investigate the changes in the distribution of laminin, and to find out cells which synthesize laminin during the organogenesis and differentiation of the lung. The fetal and neoantal rats (Sprague-Dawley strain) were used as experimental animals. The immunohisto-chemical methods were employed for detection of laminin within the developing lung tissue and the immunegold cytochemical methods were performed for detection of cells which synthesize laminin according to each stage of development. The results are as follows; 1. During fetal life, strong immunoreactivity for laminin is maintained in the basement membranes of the blood vessels and the bronchioles, the extracellular matrix of the mesenchyme, and basal lamina of the alveolar septum in the fetal rat lung. 2. After birth, laminin immunoreactivity at the alveolar septum is gradually reduced. 3. During fetal life, laminin is mainly detected within the cytoplasm of the mesenchymal cells, the endothelial cells of blood vessels and the fibroblasts in fetal rat lung. 4. According to the differentiation of type I and type II pneumocyte after birth, laminin is detected within cytoplasm of the type I pneumocytes, type II pneumocytes and fibroblasts. It is consequently suggested that laminin is largely expressed in the developing lung and laminin may be also synthesized by the type II pneumonocytes at early newborn stages.

• Applied Microscopy
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• v.39 no.1
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• pp.27-40
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• 2009

Acute respiratory distress syndrome (ARDS), also known as an acute inflammatory lung disease is developed by various factors that is originated from the destruction of alveolar-capillary barrier, and neutrophils plays an important role in the destruction. The study intended to confirm, the anti-inflammatory effect of germanium, whether a lung injury has been mitigated with the reduction of injury in alveolar-capillary barrier resulting from inhibition of neutrophils migration in lung tissue. Test groups were divided in saline administered CON, 5 hours of endotoxin administered LPS and 5 hours of endotoxin administered Ge+LPS following 1 hours of pre-processed germanium. $100{\mu}g$ endotoxin was melted in 0.5 mL saline and sprayed into airway and 26 mg germanium per 100 g weight was administered into abdominal cavity. The endotoxin group which induced an acute lung injury with administered endotoxin showed dramatic increase of pulmonary edema (p<0.001), protein contents in bronchoalveolar lavage fluid, BALF (p<0.05) and neutrophils of infiltration in BALF (p<0.001) comparing with a control group, while a pre-treated germanium group showed significant decrease in all categories comparing to the endotoxin administerd group. In the result of a microscopic observation, the structure of alveolar-capillary barrier which is constructed with basal lamina, alveolar type I cells and endothelial cell were preserved of the pre-treated germanium group relatively well compare to the endotoxin administered group. And the construction of lamellar body, microvilli and basal lamina of alveolar type II cells were also preserved relatively well. Hence, germanium activates as an anti-Inflammatory mediator in other words, it interfered neutrophils migration into lung tissue, thereby reduced injury of alveolar-capillary barrier from toxic substances of activated neutrophils. Consequently, the study has determined that the acute lung injury induced by endotoxin has been decreased by the pre-treated germanium.

• The Korean Journal of Pesticide Science
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• v.6 no.2
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• pp.96-104
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• 2002

This study was carried out to investigate cytotoxicity of paraquat on NIH 3T3 fibroblasts, toxicity of paraquat and compensatory effects of 3-methylcholanthrene (3-MC) on the rat lung. In order to conduct MIT [3-(4,5-Dimethylthiazol-2-yl) -2,5-diphenyl -2H-tetrazolium-bromide] and NR (Neutral red) assay, the $5.0{\times}10^4cell/ml$ of NIH 3T3 fibroblast in each well of 24 multi-dish were cultured. After 24 hours, the cells were treated with solution of paraquat (1, 25, 50 and $100{\mu}M$ respectively). After the NIH 3T3 fibroblast of all groups were cultured in same condition for 48 hours. MIT and NR assay were performed to evaluate the cytotoxicity of cell organelles. $MTT_{50}\;and\;NR_{50}$ of paraquat were $1668.97{\mu}M\;and\;1030.85{\mu}M$, respectively. These $IC_{50}$ of Paraquat were decided as a low cytotoxicity by Borenfreund and Puemer (1984). In order to observe the toxicity and compensatory effects of paraquat on the rat lung, Spraque Dawley male rats were used as experimental animals and were divided into paraquat only treated group and simultaneous application group of paraquat and 3-MC, at 30 min and 1, 3, 6, 12, 24, 48 and 96 hrs interval after each treatment. The animals were sacrificed by decapitation and their or the lungs were immediately removed, immersed in fixatives, and were processed with routine method for light microscopic study. Paraffin sections were stained with H&E and iron hematoxylin of Verhoeff. Under the light microscopy, erythrocytes were full in alveolar capillaries at 3 hrs and congested at 24 hrs after paraquat administration. The great alveolar cells (Type II cell) were increased and mitosis of great alveolar were observed in interalveolar septa. Many lymphocytes, macrophages and polymorphonuclear (PMN) cells were observed in connective tissue surrounding lung tissue and germinal center in lymph follicles of terminal bronchiole. Alveolar macrophages were increased in interalveolar septa and alveoli at 48 hrs. And observed many alveolar macrophages at 96 hrs. In iron hematoxylin stain of Verhoeff, Collagen fiber were increased in respiratory bronchiole, interalveolar septa and alveoli and breath of alveoli, and alveolar pore were broaden. But, in paraquat plus 3-MC treated group, morphological changes were mild in lung tissue. These results indicate that 3-MC has a compensatory effects against toxicity of paraquat by conjugation with oxygen.

• Tuberculosis and Respiratory Diseases
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• v.46 no.6
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• pp.775-785
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• 1999

Background : The herbicide paraquat can cause severe lung injury and fibrosis in experimental animals. In this study we have investigated the changes in lung endothelin-1(Et-1) levels and immunohistochemical localization in relation to treatment with cyclophosphamide and methylprednisolone in paraquat induced pulmonary fibrosis in guinea pigs. Material and methods : 29 male Hartley guinea pigs were divided into 4 groups. Group I was normal control. Paraquat was instilled into the lung of guinea pig of group II, III and IV unilaterally. Group II was treated with cyclophosphamide and methylprednisolone. Group III was treated with methlprednisolone. Group IV was not treated. The degree of fibrosis was evaluated by H-E stains and Masson's trichrome stains and cell activity was assessed by Et-1 immunohistochemical stains. Statistical evaluation was performed using the Kruskawallis oneway analysis. Results : Paraquat induced an increase in numbers of fibroblasts and total amount of lung collagen in Group IV compared to the normal controls. There was no significant difference in total numbers of fibroblasts between any of paraquat instilled groups, but there was significant increase in total amount of collagen in Group IV compared to group II and III (p<0.05). The treatment of cyclophosphamide and methyprednisolone suppressed the growths of both fibroblasts and collagen, but this suppression was stastically significant only in the case of collagen Et-1 immunoreactivities of bronchial epithelium, type II pneumocytes, endothelial cells and fibroblast in group II and III were decreased compared to those in group IV. Conclusion : These results demonstrate that Et-1 is an important contributing factor in the pathogenesis of pulmonary fibrosis. Et-1 is synthesized and released by bronchial epithelium, Type II pneumocyte, endothelial cells, alveolar macrophages and fibroblasts. Especially they are associated with alveolar macrophage and fibroblasts. We conclude that combined therapy of cyclophosphamide and methylprednisolone are more effective in the control of Et-1 expression and collagen deposition.

• Tuberculosis and Respiratory Diseases
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• v.46 no.4
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• pp.512-522
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• 1999

Background: Due to the paucity of suitable donor organs for lung allotransplantation, a number of techniques have been developed to improve the lung preservation. Ultrastructural studies of the morphologic changes of the flushing, preservation and reperfusion injury in donor lungs have rarely been reported. Methods: Adult dogs (n=46) were matched as donors and recipients for the single lung transplantation. The donor lungs were preserved after flushing with preservation solution and transplanted after 20-hours of preservation at $10^{\circ}C$. Ultrastructural features of the lung were examined after flushing, preservation and 2 hours after lung transplantation (reperfusion) respectively. Results: Electron microscopy after flushing showed focal alveolar collapse and mild swelling of type I epithelial cells. After preservation both type I epithelial cells and endothelial cells were swollen and destroyed focally. The endothelial cells showed protrusion of tactile-like structures into the lumina, blebs or vacuoles of the cytoplasm After reperfusion the lung tissue showed fibrin material in the alveoli, prominent type I epithelial cell swelling with fragmented cytoplasmic debris and marked endothelial cell swelling with vacuoles or tactile-like projections. The alveolar macrophages showed active phagocytosis. Scanning electron microscopic examination of the pulmonary parenchyma showed focally alveolar collapse and focal consolidation after the preservation and more prominent changes after the reperfusion procedure. The lungs preserved with low potassium dextran glucose solution, with additional prostaglandin $E_1(PGE_1)$ and verapamil(VP) showed relatively well preserved ultrastructures compared with those which were preserved with modified Euro-Collins or University of Wisconsin, and with additional $PGE_1$ and/or VP. Conclusion: The ultrastructural changes associated with flushing were mild in severity, the donor lungs were injured during the preservation, and further damage was occurred during the reperfusion. The reperfusion injury resulted in prominent pulmonary parenchymal alterations with a pattern of acute lung injury.

• Tuberculosis and Respiratory Diseases
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• v.66 no.5
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• pp.385-389
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• 2009

Congenital cystic adenomatoid malformation (CCAM), which is classified into five types according to size and bronchial invasion, is a rare type of developmental anomaly of the lung. CCAM is occasionally accompanied by malignancy, such as bronchioloalveolar carcinoma (BAC) or rhabdomyosarcoma. As defined by the WHO, atypical adenomatous hyperplasia (AAH) is a non-invasive spread of atypical epithelial cells in single rows along the alveolar wall, within a lesion that is usually less than 5 mm in diameter. AAH was also regarded as a pre-invasive neoplasia, especially associated with BAC and adenocarcinoma. We report a case of type II CCAM with AAH in adults, with a review of the references.

• Journal of Veterinary Science
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• v.22 no.3
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• pp.39.18-39.18
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• 2021

Background: Interferon lambda receptor 1 (IFNLR1) is a type II cytokine receptor that clings to interleukins IL-28A, IL29B, and IL-29 referred to as type III IFNs (IFN-λs). IFN-λs act through the JAK-STAT signaling pathway to exert antiviral effects related to preventing and curing an infection. Although the immune function of IFN-λs in virus invasion has been described, the molecular mechanism of IFNLR1 in that process is unclear. Objectives: The purpose of this study was to elucidate the role of IFNLR1 in the pathogenesis and treatment of porcine reproductive and respiratory syndrome virus (PRRSV). Methods: The effects of IFNLR1 on the proliferation of porcine alveolar macrophages (PAMs) during PRRSV infection were investigated using interference and overexpression methods. Results: In this study, the expressions of the IFNLR1 gene in the liver, large intestine, small intestine, kidney, and lung tissues of Dapulian pigs were significantly higher than those in Landrace pigs. It was determined that porcine IFNLR1 overexpression suppresses PRRSV replication. The qRT-PCR results revealed that overexpression of IFNLR1 upregulated antiviral and IFN-stimulated genes. IFNLR1 overexpression inhibits the proliferation of PAMs and upregulation of p-STAT1. By contrast, knockdown of IFNLR1 expression promotes PAMs proliferation. The G0/G1 phase proportion in IFNLR1-overexpressing cells increased, and the opposite change was observed in IFNLR1-underexpressing cells. After inhibition of the JAK/STAT signaling pathway, the G2/M phase proportion in the IFNLR1-overexpressing cells showed a significant increasing trend. In conclusion, overexpression of IFNLR1 induces activation of the JAK/STAT pathway, thereby inhibiting the proliferation of PAMs infected with PRRSV. Conclusion: Expression of the IFNLR1 gene has an important regulatory role in PRRSV-infected PAMs, indicating it has potential as a molecular target in developing a new strategy for the treatment of PRRSV.

• Tuberculosis and Respiratory Diseases
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• v.43 no.1
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• pp.46-53
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• 1996

Background: Endotoxin or lipopolysaccharide(LPS) can prime phagocytic cells such as polymorphonuclear leukocytes, monocytes or animal peritoneal macrophages to generate increased amounts of secretory products such as oxygen free radicals and tumor necrosis factor, which play an important role in developing adult respiratory distress syndrome in gram negative sepsis. Human alveolar macrophages(HAM) are continuously exposed to various stimuli inhaled into the alveoli, and the response to LPS might be different in HAM. Therefore, we investigated the effect of LPS pre-exposure on HAM adhered to plastic surface and A549 cell(type II human alveolar epithelial cell line) monolayer. Methods: HAM were isolated from bronchoalveolar lavage fluid from normal lung of the patients with localized lung cancer and esophageal cancer. LPS was exposed to HAM for 2hrs before or after adherence to plastic surface of 24-well Linbro plate and A549 cell monolayer. And then HAM was stimulated with PMA(phorbol myristate acetate) or fMLP(N-formyl-methionylleucyl-phenylalanine). The amount of hydrogen peroxide($H_2O_2$) production in the supernatant was measured on the principle of peroxidase-dependent oxidation of phenol red by hydrogen peroxide. Results: LPS pre-exposure could not enhance $H_2O_2$ production in neither HAM adhered to plastic surface nor one to A549 cell monolayer. But LPS even in the absence of PMA or fMLP stimulation directly increased $H_2O_2$ release in HAM if added after the adherence to A549 cell monolayer. Conclusion: Endotoxin does not prime HAM, but may directly activate HAM adhered to alveolar epithelial cells. Further investagation will be necessary.

• Tuberculosis and Respiratory Diseases
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• v.55 no.5
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• pp.478-487
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• 2003

Background : There have been several studies showing that the angiotensin II and angiotensin converting enzyme(ACE) contributes to the apoptosis of alveolar epithelial cells in idiopathic interstitial pneumonia and the activation of fibroblasts during the process of pulmonary fibrosis. These results suggest that the pulmonary fibrosis can be inhibited by the angiotensin II receptor antagonist(AGIIRA). This study was performed to identify the therapeutic effect of AGIIRA in idiopathic pulmonary fibrosis(IPF). Method : Thirteen patients with IPF, who were diagnosed with an open lung biopsy(6 patients) and furfilling the ATS criteria(7 patients) between March 1999 and October 2001 at the Gachon medical center, were enrolled in this study. Of these patients, eight patients were treated with a regimen including AGIIRA(AT group), and five were treated without AGIIRA(NT group). The pulmonary function tests and dyspnea(ATS scale) were measured at diagnosis and 1 year after treatment. All the data was collected to analyze the therapeutic effect of AGIIRA on the patients with IPF. Results : The AT group contained 8 patients(M:F=4:4) and the NT group contained 5 patients(M:F=3:2). There was no significant difference in the serum angiotensin II level between the two groups($202.5{\pm}58.5$ vs $163.7{\pm}47.3pg/ml$, p>0.05). The AT group showed an upward trend in TLC(+3%), FVC(+4%), FEV1(+3%) and DLco(+2%) compared to the NT group(TLC(-14%), FVC(-3%), FEV1(-4%) except for DLco(+5%)). The dyspnea score in the AT group improved significantly but not in the NT group. Conclusion : These results suggest that the angiotensin II receptor antagonist may have an effect on stabilizing IPF.