• The Korean Journal of Physiology and Pharmacology
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• v.13 no.3
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• pp.181-187
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• 2009

Intestinal ischemia/reperfusion (I/R) is one of common causes of acute lung injury (ALI). Early and accurate diagnosis of patients who are like to develop serious acute respiratory distress syndrome (ARDS) would give a therapeutic advantage. Ferritin and heme oxygenase-1 (HO-1) are increased by oxidative stress and are potential candidates as a predictive biomarker of ARDS. However, the mechanisms responsible for the increases of ferritin and HO-1, and their relationship to ALI, are unclear. In order to elucidate the interactions between ferritin and HO-1, we studied the changes in ferritin and HO-1 levels in serum and bronchoalveolar lavage (BAL) fluid after intestinal I/R injury in rats. Leukocyte number and protein contents in BAL fluid were elevated following I/R, and the increases were attenuated by mepacrine pretreatment. Both serum ferritin and HO-1 concentrations were progressively elevated throughout the 3 h observation period. Mepacrine pretreatment attenuated the increase of serum and BAL fluid ferritin concentrations, but did not suppress the increase of serum HO-1. Moreover, BAL fluid HO-1 levels did not change after I/R or after mepacrine pretreated I/R compared with sham rats. Unlike ferritin, HO-1 levels are not exactly matched with the ALI. Therefore, there might be a different mechanism between the changes of ferritin and HO-1 in intestinal I/R-induced ALI model.

• Natural Product Sciences
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• v.16 no.4
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• pp.245-250
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• 2010

Pulmonary pathogenesis in lupus is characterized by interstitial inflammation and vasculitis in lungs. We investigated whether bamboo culm extract (BC) attenuates pulmonary inflammation and lung injury in pristane-induced lupus mice. The pristane-induced lupus mice and healthy mice were administrated with BC 0.5 ml/kg or PBS orally once a day for 14 days. Our results demonstrated that BC significantly attenuated levels of bronchoalveolar lavage (BAL) IL-6, IL-10, IFN-$\gamma$, $PGE_2$ and VEGF, and pulmonary vascular permeability in pristane-induced lupus mice. Therefore, these findings suggest that BC may inhibit development of pulmonary inflammation and lung injury in lupus.

• Tuberculosis and Respiratory Diseases
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• v.41 no.6
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• pp.604-615
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• 1994

Background: Analysis of cells in bronchoalveolar lavage(BAL) fluid had been used to predict the histologic changes of the bronchioles and alveoli in patients with interstitial lung diseases(ILD). Definitive diagnosis can be a1so made in some cases of ILD, such as histiocytosis. However, there are a few data of the cellular components in BAL fluid in normal Korean individuals and in patients with ILD. In order to evaluate the role of the cellular analysis of BAL fluid in prediction of alveolitis and differential diagnosis among ILDs, we compared the cellular components in BAL fluid from 50 normal individuals and 86 ILD patients. Method: BAL was performed by instillation and retrievement of normal saline with fiberoptic bronchoscopy. The cell number was counted by Hemocytometer. Differential count was done up to 500 cells on slides prepared by Diff-Quik stain and non-specific esterase stain. We compared the recovery rate(RR), cell numbers(CN), and percentages of each cellular components(CP). Results: The results were as follows: 1) There was no difference in RR, CN and CP between the normal smoker group and normal non-smoker group. 2) Total cell numbers recoverd in BAL fluid increased in collagen vascular diseases(CVD), hypersensitivity pneumonitis(HP), idiopathic pulmonary fibrosis(IPF), and miliary tuberculosis(Mil TBC) groups. 3) The percentage of lymphocytes increased in HP, IPF and Mil TBC groups. Macrophage percentages increased in HP, IPF, and Mil TBC groups. Neutrophil percentages were increased in CVD, HP, IPF and Mil TBC groups. Eosinophil percentages were increased in HP, IPF and Mil TBC groups. The numbers of each cells showed same findings as the percentages did. Conclusion: The analysis of cellular components of BAL fluid can predict the presence of alveolitis in many cases of ILDs. However, It was not helpful in differential diagnosis among ILDs.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.254-254
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• 1996

Eosinophils are known to be important effector cells in pathogenesis of asthma. The elucidation of mechanism by which eosinophil survival is regulated in vivo at sites of inflammation is critical tn our understanding of asthma pathogenesis. The maintenance of these cells at site of inflammation depends upon tile balance between its tendency to undergo apoptosis and tile local eosinophil-viability enhancing activity, Qualitative and quantative phenotypic differences have been observed between bronchoalveolar lavage (BAL) and peripheral blood (PB) eosinophils (EOS). We hypothesize that BAL EOS Possess altered functional feature compared to PB EOS. BAL and PB EOS were obtained from ragweed allergic asthmatics after segmental antigen challenge (SAC) at 24 hour or one week, and purified over percoll and CDl6 negative selection. Cells were cultured in duplicate in RPMI, 15% FCS and 1% penicillin/streptomycin without exogenous cytokines. Eosinophil purity and viability was >92%. BAL. EOS viability was 69${\pm}$4.4% versus 39${\pm}$1.6% for PB EOS (p<0.005) at 48 hour time point, and this difference was maintained through day 5 (32${\pm}$7.6% vs. 3.0${\pm}$ 1.4%, p<0.05), Among BAL EOS, those harvested one week after SAC appeared to have an prolonged survival compared to those harvested at 24 hour. Coculture of BAL and PB EOS resulted in significant viability enhancement than expecteed. Direct neutralization of GM-CSF activity, not IL-3 and EL-5, markedly decreased tile survival of BAL EOS in culture, and abrogated tile viability enhancing activity of their culture supernatants in a dose dependent manner. We conclude that BAL EOS activated in vivo possess enhanced viability compared to PB EOS. Mixing and neutralization experiments suggest a role for autocrine production of GM-CSF.

• Journal of Korean Society for Atmospheric Environment
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• v.18 no.E2
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• pp.121-128
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• 2002

This study was carried out to investigate if nitric oxide synthase (NOS) inhibitors modulate airway inflammation induced by diesel exhaust particles (DEP). N$\^$G/-nitro-L-arginine methyl ester (L-NAME), a potent constitutive NOS (cNOS) inhibitor, and aminoguanidine (AG), a selective inducible NOS (iNOS) inhibitor, were administered to mice in their drinking water for 7 weeks. Airway inflammation was elicited by the repeated intratracheal administration of DEP. The results showed that macrophages, inflammatory eosinophils and neutrophils in bronchoalveolar lavage (BAL) fluids by intratracheal DEP instillation were significantly suppressed in the mice treated with two NOS inhibitors toghther with DEP. The suppression of these cells was more effective in AG treated groups than in L -NAME treated groups. NOS inhibitor treatment also reduced interleukin -5 (IL-5 in the BAL fluids and lung homogenates. Additionally, it was found that eosinophil peroxidase (EPO) activity in the BAL fluids was also decreased by NOS inhibitor treatment. These results suggest that nitric oxide (NO) is produced in airway inflammation by repeated DEP instillation, and that iNOS inhibition as well as cNOS inhibition can play a modulating role in this airway inflammation by DEP.

• Toxicological Research
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• v.18 no.2
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• pp.159-165
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• 2002

Recently, we reported (korean J. Biomed. Lab. Sci., 6(4): 245-251, 2000) that cyclohexane (l.56 g/kg of body wt., i.p.) administration led to lung injury in rats. However the detailed mechanism remain to be elucidated. This study was designed to clarify the mechanism of lung damage induced by cyclohexane in rats. First, lung damage was assessed by quantifying bronchoalveolar lavage fluid (BAL) protein content as well us by histopathological examination. Second, activities of serum xanthine oxidase (XO), pulmonary XO and oxygen free radical scavenging enzymes. XO tope conversion (O/D + O, %) ratio and content of reduced glutathione (GSH) were determined. In the histopathological findings, the vasodilation, local edema and hemorrhage were demonstrated in alveoli of lung. And vascular lumens filled with lipid droplets, increased macrophages in luminal margin and increased fibroblast-like interstitial cells in interstitial space were observed in electron micrographs. The introperitoneal treatment of cyclohexane dramatically increased BAL protein by 21-fold compared with control. Cyclohexane administration to rats led to a significant rise of serum and pulmonary XO activities and O/D + O ratio by 47%,30% and 24%, respectively, compared witれ control. Furthermore, activities of pulmonary oxygen free radical scavenging enzymes such as superoxide dismutase, glutathione peroxidase and glutathione S-transferase, and GSH content were not found to be statistically different between control and cyclohexane-treated rats. These results indicate that intraperitoneal injection of cyclohexane to rats may induce the lipid embolism in pulmonary blood vessel and lead to the hypoxia with the ensuing of oxygen free radical generation, and which may be responsible for the pulmonary injury.

• 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.61 no.6
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• pp.562-566
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• 2006

Fat embolism syndrome is a rare clinical diagnosis of dyspnea with acute respiratory failure and neurological signs caused by a traumatic long bone fracture. We report a case of fat embolism in a 22 year-old man after a traffic accident. Dyspnea and stuporous mental changes developed on the $1^{st}$ day after the external fixation operation of a left metaphyseal femur fracture. On the following day, he was transferred from a hospital to this one because of acute respiratory failure. After recovery, macrophages with fat droplets were found in the bronchoalveolar lavage fluid 1. It is important to diagnose a fat embolism as the correct cause of acute respiratory failure through the BAL in the acute state of fat embolism syndrome It is believed that clinically apparent or sometimes hidden fat embolism syndrome can be diagnosed from the BAL during the recovery state.

• Journal of Environmental Health Sciences
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• v.39 no.1
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• pp.48-55
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• 2013

Objective: The use of nanoparticle products is expected to present a potential harmful effect on consumers. Also, the lack of information regarding inhaled nanoparticles may pose a serious problem. In this study, we addressed this issue by studying pulmonary toxicity after nasal instillation of Al-NPs in SD rats. Methods: The animals were exposed to Al-NPs at 1 mg/kg body weight (low dose), 20 mg/kg body weight (medium dose) and 40 mg/kg body weight (high dose). To determine pulmonary toxicity, bronchoalveolar lavage (ts.AnBAL) fluid analysis and histopathological examination were conducted in rats. In addition, cell viability was investigated at 24 hours after the treatment with Al-NPs. Results: BAL fluid analysis showed that total cells (TC) count and total protein (TP) concentrations increased significantly in all treatment groups, approximately two to three times. Also, lactate dehydrogenase (LDH) and cytokines such as TNF-alpha and IL-6 dose-dependently increased following nasal instillation of Al-NPs. However, polymorphonuclear leukocytes (PMNs) levels showed no significant changes in a dose dependant manner in BAL fluid. In the cytotoxicity analysis, the treatment of Al-NPs significantly and dose-dependently induced cell viability loss (20 to 30%) and damage of cell membrane (5 to 10%) in rat normal lung epithelial cells (L2). Conclusions: Our results suggest that inhaled Al-NPs in the lungs may be removed quickly by alveolar macrophages with minimal inflammatory reaction, but Al-NPs have the potential to affect lung permeability. Therefore, extensive toxicity evaluations of Al-NPs are required prior to their practical application as consumer products.

• The Journal of Pediatrics of Korean Medicine
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• v.20 no.1
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• pp.181-194
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• 2006

Objective : Author evaluate the effects of Citri Reticulatae Viride Pericarpium for the bronchial asthma using assesment of the vascular endothelial growth factor after Citri Reticulatae Viride Peicarpium was intravenously administered Ovalbumine(OVA)-sensitized and -challenged mice. Material and Methods : Twenty-four female mice, 8-10 weeks old and free of murine specific pathogens, were sensitized by intraperitoneal injection of OVA. Of the sensitized mice, ten mice didn't administrate Citri Reticulatae Viride Pericarpium and the other ten mice administrated Citri Reticulatae Viride Pericarpium. Mice were sensitized on the first and fourteen days introspectional injection of 20 ${\mu}g$ OVA. After$21^{st}\;22^{th}\;and\;23^{rd}$, the initial sensitization, the mice were challenged for 30 minutes with an aerosol of 1% OVA in saline. Citri Reticulatae Viride Pericarpium administered 200mg/kg in the tail of the mouse, one a day, for 7 days and beginning 14 days after first sensitization. Bronchoalveolar lavage was performed 72 hours after the last challenge, and total cell numbers in the BAL fluid were count. Also, lever of VEGF in the BAL fluid was measured by Enzyme immunoassays and Western blot analysis. Results: Total cell numbers in BAL fluid were significantly greater than from 72 hrs after OVA inhalation compared with cell numbers in the control group. However, there was no difference of the total cell numbers between OVA-challenge groups without Citri Reticulatae Viride Pericarpium, and OVA-challenge with Citri Reticulatae Viride Pericarpium. Enzyme immunoassay revealed that VEGF levels in the BAL fluids were significantly increased 72 hrs after OVA inhalation compared with levels in the control group. After administration of the Citri Reticulatae Viride Pericarpiu, the levels of the VEGF in BAL fluids 72 hrs after OVA inhalation reduced dramatically. Western blot analysis revealed that VEGF protein levels were increased in the all mice which were challenge with OVA, without administered Citri Reticulatae Viride Pericarpium, compared the normal mouse. However, in the groups of the administered Citri Reticulatae Viride Pericarpium, the VEGF protein level markedly decreased. Conclusion: Citri Reticulatae Viride Pericarpium might affect the treatment of the bronchial ashma as a inhibition of the VEGF.