• Tuberculosis and Respiratory Diseases
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• v.38 no.2
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• pp.143-154
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• 1991

Pneumconiosis is a sort of pulmonary fibrosis consequent to the inhalation of the respirable dusts. Thus, the pathogenesis of silicosis have concentrated largely on the early response of alveolar macrophage and the later fibroblastic stimulation. But the role of the other cells and continuing cell injury in the pathogenesis has not been fully studied. And the chemical factors such as prostaglandin, fibroblast stimulating factor and inhibiting factor and chemotaxin are also participated in the mechanism of pulmonary fibrosis in silicosis. In order to clarify the role of alveolar cells and prostaglandin, we investigated the changes of the cellularities in bronchoalveolar lavage fluid and tissue pathology in the experimental silicosis with the time sequence. The experimental animals were divided into 3 groups; control group received only intratracheal injection of 0.5 ml saline, silica group received the intratracheal instillation of 40 mg silica with the same amount saline, and aspirin group received 450 mg/kg of aspirin after silica instillation. The results were as follows: 1) The total cells of bronchoalveolar lavage fluid in the silica group markedly increased in comparison with the control group, but there was no significant difference between the silica and aspirin groups. 2) The percentages of alveolar macrophages to the total number of cells in the silica group tended to be lower than those in the control group and also lower than those in the aspirin group at the 1st week after silica instillation. 3) The percentages of neutrophils to the total number of cells in the silica group were significantly higher than those in the control group during the entire period and also higher than those in the aspirin group at the 3rd day after silica instillation. 4) In the silica group, the percentages of lymphocytes to the total number of cells were increased 143 progressively with the time course and those were significantly higher than those in the control group from the 3rd week after silica administration. There were marked differences of lymphocyte percentages between the silica and aspirin groups at the 1st week after silica instillation. 5) The inflammatory change was observed in the rat lung at the 1st day after silica instillation. Also the silicotic nodule appeared in the silica group at the 1st week but we could not find out that nodule in the aspirin group at that time. The fibrotic changes in the rat lung tended to be increased progressively with the time course, therefore, the diffuse fibrotic pattern appeared in the whole field at the 20th week after silica instillation. 6) By the electron microscopy, there were gradual increases of phagosomes and vacuoles in the alveolar macrophage in the silica group as compared with the control group. These results suggest that the neutrophils and the lymphocytes have also participated in the pulmonary fibrosis even though the alveolar macrophage has a major role, and prostaglandin mediate the inflammation and pulmanary fibrosis in the experimental silicosis.

• Journal of Preventive Medicine and Public Health
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• v.32 no.4
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• pp.467-472
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• 1999

Objectives: This study was conducted to evaluate the cytotoxicity of gallium arsenide(GaAs), indium phosphide(InP) and indium arsenide(InAs) all of which are used a$ the semiconductor eletments in semiconductor industry. Methods: Cytotoxicity id the alveolar macrophage was evaluated by the measurement of in vitro magnetometry, LDH release assay and histological examination. Results: The relaxation curves by the in vitro magnetometry showed that GaAs has the cytotoxicity for the alveolar macrophage which is more significant in the higher dosages, while this cytotoxicity is not appeared in the groups added with InP or InAs or PBS. In the decay constant for two minutes after magnetization, GaAs-added groups showed a significant decrease with increasing doses, but both InP- and InAs-added groups did not show any significance. The LDH release assay showed a dose-dependent increasing tendency in the GaAs-, InP- and InAs-added groups. In terms of cellular morphological changes, GaAs-added groups revealed such severe cellular damages as prominent destructions in cell membranes and their morphological changes of nucleus, while InP- and InAs-added groups remained intact in intracellular structures, except for cytoplasmic degenerations. Conclusions: It is suggested that GaAs is more influential to cytotoxicity of alveolar macrophages than InP and InAs.

• 대한상한금궤의학회지
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• v.13 no.1
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• pp.21-44
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• 2021

Objective : This study aimed to assess the preventive effect of Bupleuri Radix aqueous extracts (BR) and red koji-fermented BR (fBR) in lipopolysaccharide (LPS)-induced acute lung injury in a rat model. Methods : Rats were administered 30, 60, or 120 mg/kg/day of fBR for 28 days before LPS treatments. All rats were sacrificed 5 h after LPS treatment (500 ㎍/head, intratracheal instillation). Body weights, lung weights, pulmonary transcapillary albumin transit, arterial gas parameters (pH, partial pressure [Pa] of O2, PaCO2), bronchoalveolar lavage fluid (BALF) protein, lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), total cell numbers, neutrophil/alveolar macrophage ratios, lung malondialdehyde (MDA), and myeloperoxidase (MPO) were measured. In addition, histopathological changes including the luminal surface of alveoli (LSA), thickness of alveolar septum, and number of polymorphonuclear neutrophils (PMNs) were checked. Results : LPS injection led to increases in lung weights, pulmonary transcapillary albumin transit, BALF protein, LDH, TNF-α and IL-1β contents, total cells, neutrophil and alveolar macrophage ratios, lung MDA, MPO, alveolar septum thickness, and PMNs, and decreases in PaCO2 and pH of arterial blood and LSA. However, these LPS-induced acute lung injuries were inhibited by pretreatment of 30, 60, and 120 mg/kg of fBR. The most favorable effects were seen with 30 mg/kg fBR as compared with 60 mg/kg of α-lipoic acid and BR. Conclusions : fBR showed preventive effects on LPS-induced acute lung injury, which resembles acute respiratory distress syndrome. The mechanisms of action were likely via antioxidant and anti-inflammatory means.

• Korean Journal of Veterinary Research
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• v.36 no.1
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• pp.131-142
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• 1996

The effect of relative humidity in swine house on swin pleuropneumonia was examined in piglets experimentally infected with Actinobacillus pleuropneumoniae serotype 5. A total of 20 piglet were grown under 30~40%, 41~50%, 51~64% and 65~80% relative humidity chambers after intratracheal inoculation of A pleuropneumoniae. Characteristic fibrinous pleuropneumonia was observed in the pigs grown at the low relative humidity groups. The detailed results were as follows : 1. Growth performance and environment conditions were lower than high relative humidity groups. 2. Characteristic histopathological findings were fibrinous pleuritis and pneumonia accompanied congestion, hemorrhage, thrombosis and edematous change. 3. Antigenic distribution of inoculated bacterium was found mainly in alveolar macrophages or accumulated foci of macrophages adjacent to necrotic area. 4. Characteristic electron microscopic findings were proliferation of type II pneumocyte with increased lamella bodies and activated alveolar macrophages with pseudopods and widening of interstitium.

• Korean Journal of Veterinary Research
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• v.37 no.1
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• pp.177-183
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• 1997

One cytopathogenic virus was isolated in alveolar macrophages from pig without any apparent respiratory clinical signs. Biophysical properties and electron microscopy of the isolate showed the characteristics of adenovirus. Intracytoplasmic inclusion bodies were seen in virus-inoculated cells. The genetic analysis indicated the presence of DNA with the size of >20Kb. In a serological survey of 40 serum samples collected from two different farms in slaughter house, 9 sera were positive for neutralizing antibody against the isolate. The potential implications of the isolate as the causative agent in respiratory disorder were discussed.

• The Korean Journal of Physiology
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• v.29 no.1
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• pp.1-11
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• 1995

Alveolar macrophages play a pivotal role in the pathogenesis of silicosis since the macrophages may release a wide variety of toxic and inflammatory mediators as well as mitogenic growth factors. In the present study, the effects of in vitro exposure to silica on release of various mediator such as reactive oxygen species, platelet activating factor(PAF), and interleukin-1 (IL-1) by alveolar macrophages were examined. First, hydrogen peroxide release from alveolar macrophages was monitored by measuring the change in fluorescence of scopoletin in the absence or presence of graded concentration of silica. Significantly enhanced release of hydrogen peroxide was observed at 0.5 mg/ml and above. A maximal enhancement of 10 fold above control was observed at 5 mg/ml silica. Similarly, in vitro exposure to silica also significantly stimulated the generation of chemiluminescence from alveolar macrophages at 0.5 mg/ml and above with n maximal enhancement of 8 fold at 5 mg/ml silica. Second, PAF release from alveolar macrophages after 30 min incubation at $37^{\circ}C$ in absence or presence of zymosan and silica was determined by measuring $^{3}H-serotonin$ release ability of the conditioned macrophage supernates from platelets. 5 mg/ml zymosan as a positive control fur the PAF assay increased PAF release by 19 % of total serotonin release. Furthermore, silica also resulted in significant enhancement of the PAF release compared with that in unstimulated (control) cells, i.e., $17.7{\pm}5.8%$ and $24.0{\pm}4.9%$ of total serotonin release at 5 mg/ml and 10 mg/ml silica, respectively, which represents the release of nanomole levels of PAF. Lastly, IL-1 production by alveolar macrophages was analysed following their stimulation with lipopolysaccharide (LPS) and silica by their capacity to stimulate thymocyte proliferation. $10\;{\mu}g/ml$ LPS resulted in an 11 fold increase in IL-1 production. In comparison, $50\;{\mu}g/ml$ silica resulted in a 4 fold increase in IL-1 release. These data indicate that in vitro exposure of alveolar macrophages to silica activates the release of various bioactive mediators such as reactive oxygen species, PAF and IL-1 which thus contribute to amplification of inflammatory reactions and regulation of fibrotic responses by the lung after inhalation of silica.

• Tuberculosis and Respiratory Diseases
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• v.43 no.6
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• pp.936-944
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• 1996

Background: Neutrophils or monocytes separated in vitro by the adherence to plastic surface are known to be activated by surface adherence itself and subsequent experimental data might be altered by surface adherence. Adhesion molecules and gene transcription of the inflammatory mediators are known to be associated in this process. To evaluate whether adhesion molecule and transcriptional activation of the inflammatory substances are also involved in the activation of human alveolar macrophage by the adherence procedure, we designed this experiment. Method : Bronchoalveolar lavage was performed in the person whose lung of either side was confirmed to be nonnal by chest cr and alveolar macrophage was harvested. To measure the expression of Interleukin-8(IL-8) mRNA, manganese superoxide dismutase(SOD) mRNA and CD11/CD18 mRNA in human alveolar macrophage of both adherence state and suspension state, Northern blot analysis was done at 0, 2, 4, 8 and 24hrs after the adherence to plastic surface and during suspension state. Then, phorbol myristate acetate(pMA) and N-formyl-methionyl-leucyl-phenylalanine(fMLP) were added respectively in the same experimental condition. Result : 1) Human alveolar macrophages in the adherent state induced IL-8 mRNA and SOD mRNA expression which was maximal at 8 hours after the adherence to plastic surface. But we could not observe the upregulation of CD18 mRNA by surface adherence. 2) PMA induced these mRNA expression both in the adherent cell and the nonadherem cells, but the induction of mRNA expression by fMLP occurred only in the adherent cells. Conclusion: These results suggest that adherence of huamn alveolar macropahge is an important cell-activating event that may play a critical role in the modulation of lung inflammatory respones.

• Journal of Food Hygiene and Safety
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• v.8 no.4
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• pp.181-188
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• 1993

It is well known that bacterial lipopolysaccharide (LPS) stimulates the prostaglandin (PG) synthesis in various experimental system, but the mechanism and the detailed nature of its action are yet to be understood. Thus, this study was designed to characterize LPS induced PG synthesis in rat alveolar macrophage. Although results were not so much prominent, LPS stimulated PGE2 synthesis in macrophage with short term exposure, and this was thought to be mainly due to the activation of phopholipase A2+ But there was a burst in the PG synthesis 6 hours after the LPS treatment and this was accompanied with the increase of cyclooxygenase activity. This effect was not mediated by tumor necrosis factor (TNF) or platelet activating factor (PAF), and the existence of serum was prerequisite for its action. Growth factors such as epidermal growth factor (EGF) and platelet derived growth factor (PDGF) themselves did not stimulate PG synthesis and the showed stimulatory activities to some extent. Normal rat serum was more effective for the elicitation of the LPS action than growth factors. Thus, considering the amounts of growth fafctors contained in normal serum, it was suggested that another factors like LPS binding protein (LBP) might be involved in the serum effect on LPS action. Conclusively. it was thought that LPS could stimulate PG synthesis through interaction with serum factors such as EGF, PDGF and/or LBP.

• Clinical and Experimental Pediatrics
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• v.46 no.6
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• pp.536-540
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• 2003

Purpose : Aspiration of foreign material into the lungs can cause acute or chronic pulmonary diseases. It is difficult to detect small amounts of aspiration due to the lack of safe, sensitive and specific diagnostic tests. Recently, in animal or human studies, it has been reported that immunochemistry for lactalbumin can be used to detect the minimal aspiration. So, the authors' investigation was designed to determine whether human milk phagocytized alveolar macrophages can be detected in human milk aspirated mice. Methods : Sixty four male mice, 6-8 weeks old and 30-40 gm weighing, were used for this study. About 0.05 mL of human milk or normal saline were given intranasally once per day for 1 day or 3 days. Under anesthesia with ketamine and xylazine, the trachea of each mouse was cannulated with an 18G Jelco needle and then, each mouse's lungs were lavaged three times with 0.5 mL of phosphate buffer solution at 2, 8, 24, and 48 hours after the last milk or normal saline instillation. Cells in bronchoalveolar lavage fluid were stained with Oil Red O and immunocytochemistry for alpha-lactalbumin. Results : Immunocytochemical reactivity for alpha-lactalbumin or lipid-laden alveolar macrophages were not observed in the normal saline aspirated groups. Immunocytochemical reactivity for alpha-lactalbumin were observed in the human milk aspirated groups. They showed a peak at 8 hours and decreased markedly at 24 hours but persisted even at 48 hours after aspiration. Immunocytochemical stain positive alveolar macrophages were noted similarly in number between single and multiple aspiration groups. Conclusion : These observations suggested that alveolar macrophages for lactalbumin could be more easily detected on immunocytochemistry than Oil Red O stain, and immunocytochemistry could be used as a sensitive and specific diagnostic test for the detection of human milk aspiration.

• IMMUNE NETWORK
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• v.23 no.5
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• pp.42.1-42.21
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• 2023

When the lungs are infected with bacteria, alveolar macrophages (AMs) are recruited to the site and play a crucial role in protecting the host by reducing excessive lung inflammation. However, the regulatory mechanisms that trigger the recruitment of AMs to lung alveoli during an infection are still not fully understood. In this study, we identified a critical role for NADPH oxidase 4 (NOX4) in the recruitment of AMs during Staphylococcus aureus lung infection. We found that NOX4 knockout (KO) mice showed decreased recruitment of AMs and increased lung neutrophils and injury in response to S. aureus infection compared to wildtype (WT) mice. Interestingly, the burden of S. aureus in the lungs was not different between NOX4 KO and WT mice. Furthermore, we observed that depletion of AMs in WT mice during S. aureus infection increased the number of neutrophils and lung injury to a similar level as that observed in NOX4 KO mice. Additionally, we found that expression of intercellular adhesion molecule-1 (ICAM1) in NOX4 KO mice-derived lung endothelial cells was lower than that in WT mice-derived endothelial cells. Therefore, we conclude that NOX4 plays a crucial role in inducing the recruitment of AMs by controlling ICAM1 expression in lung endothelial cells, which is responsible for resolving lung inflammation during acute S. aureus infection.