• Tuberculosis and Respiratory Diseases
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• v.41 no.1
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• pp.11-19
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• 1994

Background: Mycobacterium tuberculosis is a facultative intracellular pathogen which persists and multiplies within macrophage. Competent cell mediated immunity by cooperation of both T lymphocyte and macrophage of the host is required to kill the Mycobacterium tuberculosis. But a precise understanding of the pathogenesis of tuberculosis infection in pulmonary alveolar macrophage has not been achived. Research on the macrophage's basic microbicidal mechanism has elucidated the importance of oxygen-dependent or oxygen-independent components. Oxygen dependent processing begins with the reduction of oxygen by NADPH oxidase and generation of superoxide. In this study, the oxidative metabolic status of blood monocyte and pulmonary alveolar macrophage in patients with active pulmonary tuberculosis was accessed and compared with that of healthy control subjects to know whether there was a basic difference in superoxide generation by mononuclear cells between two groups. Methods: Pulmonary alveolar macrophage was purified after performing BAL(bronchoalveolar lavage) through the bronchi of infected lesion by plastic adhesion method. Blood monocyte was purified by Ficoll-Hypaque method. Superoxide generation by blood monocyte and pulmonary alveolar macrophage was measured by ferricytochrome-C reduction method after either stimulated with PMA(phorbol myristate acerate) or non-stimulated states. We also measured the effect of pulmonary tuberculosis patient's serum on superoxide generation by monocyte. Results: 1) Generation of superoxide by alveolar macrophage obtained from patients with pulmonary tuberculosis was little higher than those of controls, and PMA enhanced the generation of 2) Generation of superoxide by blood monocyte obtained from patients with pulmonary tuberculosis was little higher than those of control(p>0.05), and PMA more enhanced the generation of superoxide in patientswith pulmonary tuberculosis than those in controls(p<0.02). 3) Patient's serum enhanced the generation of superoxide by blood monocyte obtained from patients with pulmonary tuberculosis and controls, but not in the case of PMA stimulated blood monocyte. Conclusion: The present study suggest that the phenomenon of M.tuberculosis escape the microbicidal action of macrophage was not result of suppressed superoxide generation by blood monocyte and pulmonary alveolar macrophage, rather there might be a factor to stimulate the generation of superoxide by blood monocyte in pulmonary tuberculosis patient serum, but the comparision with effect of control's serum on superoxide generation needs further elucidation.

• Tuberculosis and Respiratory Diseases
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• v.67 no.6
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• pp.569-573
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• 2009

Idiopathic pulmonary alveolar proteinosis (PAP) is a rare disorder characterized by surfactant component accumulation in the alveolar space. Idiopathic PAP has recently been recognized as a autoimmune disease of impaired alveolar macrophage function caused by autoantibodies against granulocyte-macrophage colony-stimulating factor (GM-CSF). While whole lung lavage has been the standard treatment, not every patient shows a complete response. Subcutaneous injection or inhalation of GM-CSF is another promising treatment option for PAP. A 45-year-old patient visited our hospital for dyspnea, he was diagnosed as PAP and underwent whole lung lavage. Eighteen months later, the patient had not achieved complete remission in despite of initial response. After then he was administered with GM-CSF (5 ${mu}g/kg/day$, subcutaneous injection) for fivetimes a week during 2 months. Nine months later, the abnormal shadows in high-resolution computed tomography (HRCT) decreased and the patient fully recovered in forced vital capacity. After 60 months, the HRCT scan showed complete remission of PAP.

• Korean Journal of Veterinary Service
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• v.21 no.1
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• pp.41-56
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• 1998

These experiment was carried out to investigate the pulmonary lesions and the function of alveolar macrophages in rats exposed to cement dusts. 1. The number of total cells in bronchoalveolar lavage fluid(BAL) increased remarkably in 1st month. As time goes by, tend to less and less in numbers. 2. The number of neutrophil and lymphocytes obtaining from the total cell of BAL increased remarkably in first month, but as time goes by, they tended to grow less and less in number. Macrophages decreased gradually after being temporarily augmentation. 3. Histipathologically, the thickening of alveolar walls, alveolar interstitial, and infiltrated macrophages containing cement dusts.

• Journal of Yeungnam Medical Science
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• v.27 no.1
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• pp.57-62
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• 2010

Pulmonary alveolar proteinosis (PAP) is a rare disorder that's characterized by accumulation of surfactant components in the alveolar space. Idiopathic PAP is recognized as an autoimmune disease that's due to impaired alveolar macrophage function and this caused by autoantibodies against granulocyte-macrophage colony-stimulating factor (GM-CSF). We report here a case of pulmonary alveolar proteinosis that was deemed interstitial lung disease at the initial diagnosis. A 61-year-old man presented with intermittent blood tinged sputum and dyspnea on exertion. The man was a painter for 30 years and he had a 10 pack-years smoking history. Chest computerized tomography (CT) revealed multifocal ground-glass opacity with interstitial thickening at both lungs. His pulmonary function tests and methacholine test revealed non specific results. He was diagnosed with interstitial lung disease on the basis of the chest CT finding and occupational history. However, seven months later, his symptoms progressed. Follow-up chest CT was performed. Wedge resection via video-assisted thoracoscopic surgery (the anterior basal segment of the left lower lobe) was done. Microscopic examination showed large groups of alveoli with excessive amounts of surfactant and a complex mixture of protein and lipid (fat) molecules. Finally, he was diagnosed as having pulmonary alveolar proteinosis.

• Molecules and Cells
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• v.44 no.5
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• pp.292-300
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• 2021

Macrophages residing in various tissue types are unique in terms of their anatomical locations, ontogenies, developmental pathways, gene expression patterns, and immunological functions. Alveolar macrophages (AMs) reside in the alveolar lumen of the lungs and serve as the first line of defense for the respiratory tract. The immunological functions of AMs are implicated in the pathogenesis of various pulmonary diseases such as allergic asthma, chronic obstructive pulmonary disorder (COPD), pulmonary alveolar proteinosis (PAP), viral infection, and bacterial infection. Thus, the molecular mechanisms driving the development and function of AMs have been extensively investigated. In this review article, we discuss the roles of granulocyte-macrophage colony-stimulating factor (GM-CSF) and transforming growth factor (TGF)-β in AM development, and provide an overview of the anti-inflammatory and pro-inflammatory functions of AMs in various contexts. Notably, we examine the relationships between the metabolic status of AMs and their development processes and functions. We hope that this review will provide new information and insight into AM development and function.

• Proceedings of the Korean Society of Toxicology Conference
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• 2005.05a
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• pp.51-82
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• 2005

To compare the pulmonary toxicity between ultrafine colloidal silica particles (UFCSs) and fine colloidal silica particles (FCSs), mice were intratracheally instilled with 3 mg of 14-nm UFCSs and 230-nm FCSs and pathologically examined from 30 mill to 24 hr post-exposure. Histopathologically, lungs exposed to both sizes of particles showed bronchiolar degeneration and necrosis, neutrophilic inflammation in alveoli with alveolar type II cell proliferation and particle-laden alveolar macrophage accumulation. UFCSs, however, induced extensive alveolar hemorrhage compared to FCSs from 30 min onwards. UFCSs also caused more severe bronchiolar epithelial cell necrosis and neutrophil influx in alveoli than FCSs at 12 and 24 hr post-exposure. Laminin positive immunolabellings in basement membranes of bronchioles and alveoli of UFCSs treated animals was weaker than those of FCSs treated animals in all observation times. Electron microscopy demonstrated UFCSs and FCSs on bronchiolar and alveolar wall surface as well as in the cytoplasm of alveolar epithelial cells, alveolar macrophages and neutrophils. Type I alveolar epithelial cell erosion with basement membrane damage in UFCSs treated animals was more severe than those in FCSs treated animals. At 12 and 24 hr post-exposure, bronchiolar epithelia cells in UFCSs treated animals showed more intense vacuolation and necrosis compared to FCSs treated animals. These findings suggest that UFCSs has greater ability to induce lung inflammation and tissue damages than FCSs.

• 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.

• Toxicological Research
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• v.9 no.2
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• pp.241-251
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• 1993

Present studies were carried out in order to estabilish the bronchoalveolar lavage method and to examine the response of bleomycin and peplomycin on the total cell number and the subpoulations of bronchoalveolar lavage fluid. A total of 24 male F344 rats, weighing 300-350 mg, were divided into 3 groups. Animals recelved either belomycin (BLM` 0.75 mg/0.2 ml/rat), peplomycin (PLM` 0.25mg/0.2ml/rat) for groups 2 and 3 or an equal volume of sterile saline lacking drugs for controls (group 1).

• 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.

• Applied Microscopy
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• v.31 no.3
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• pp.275-285
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• 2001

The pulmonary alveolar macrophage is thought to play an important role in the mediation of acute inflammatory lung injury by secretory products including degraded enzymes, cytokines, and reactive oxygen metabolites . This study was conceived to understand the role of alveolar macrophage in oxidative stress induced acute lung injury. To examine the alveolar macrophages and xanthine oxidase (XO) activity in bronchoalveolar lavage fluid (BALF), time-dependent changes of numbers of alveolar macrophages, monocytes and neutrophils in alveolar cavity were counted in association with ultrastructural and cytochemical observations of lung tissue and alveolar cells. The number of monocytes was increased (p<0.001) at 1h after IL-1 treatment compared with that of sham. At 2h after instillation of IL-1, the number of alveolar macrophages was the highest, XO activity in BALF was elevated at 2h after IL-1 instillation and the activity was markedly elevated(p<0.05) at 3h after IL-1 treatment. On the basis of these experimental results, it is suggested that, during early phase of acute lung injury induced by IL-1, alveolar macrophage-derived XO contributes to lung injury earlier than the neutrophilic respiratory burst.