Serum Calprotectin Is a Potential Marker in Patients with Asthma

Background@#Calprotectin is the major cytosolic protein in neutrophil granulocytes.Although asthma is known to cause eosinophilic inflammation, some patients with asthma have non-eosinophilic inflammation, which is characterized by local neutrophilic inflammation. The aim of this study was to assess calprotectin expression levels in a mouse model of asthma, and to observe the relationship of serum calprotectin level and clinical variables in patients with asthma. @*Methods@#Mice were sensitized and challenged with 10 μg and 20 μg of Aspergillus fumigatus, respectively; mice treated with saline were used as a control. The levels of calprotectin were determined using enzyme-linked immunosorbent assay, immunoblotting, and immunohistochemical analysis. The serum levels of calprotectin were also assessed in patients with asthma. The relationship between calprotectin and clinicopathological characteristics was determined. @*Results@#Calprotectin, S100A8, and S100A9 expression was elevated in the mouse lungs, Calprotectin levels were higher in the serum of patients with asthma (n = 33) compared with those of healthy individuals (n = 28). Calprotectin levels correlated with forced expiratory volume in one second/forced vital capacity (r = −0.215, P = 0.043), smoke amount (r = 0.413, P = 0.017), body mass index (r = −0.445,P= 0.000), and blood neutrophil percentage (r = 0.300, P = 0.004) in patients with asthma. @*Conclusion@#Our data suggest that calprotectin could potentially be used as a biomarker for asthma.

Apolipoprotein A1 Inhibits TGF-β1-Induced Epithelial-to-Mesenchymal Transition of Alveolar Epithelial Cells / 결핵및호흡기질환

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor β1 (TGF-β1)-induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we determine whether ApoA1 modulates TGF-β1-induced EMT in experimental lung fibrosis and clarify its mechanism of action. METHODS: The A549 alveolar epithelial cell line was treated with TGF-β1 with or without ApoA1. Morphological changes and expression of EMT-related markers, including E-cadherin, N-cadherin, and α-smooth muscle actin were evaluated. Expressions of Smad and non-Smad mediators and TGF-β1 receptor type 1 (TβRI) and type 2 (TβRII) were measured. The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice. RESULTS: TGF-β1-treated A549 cells were changed to the mesenchymal morphology with less E-cadherin and more N-cadherin expression. The addition of ApoA1 inhibited the TGF-β1-induced change of the EMT phenotype. ApoA1 inhibited the TGF-β1-induced increase in the phosphorylation of Smad2 and 3 as well as that of ERK and p38 mitogen-activated protein kinase mediators. In addition, ApoA1 reduced the TGF-β1-induced increase in TβRI and TβRII expression. In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium. CONCLUSION: Our data demonstrate that ApoA1 inhibits TGF-β1-induced EMT in experimental lung fibrosis.

Gene-Gene Interaction Between CCR3 and Eotaxin Genes: The Relationship With Blood Eosinophilia in Asthma

PURPOSE: Eosinophils function as an effector cell in the development of asthma and allergic disease. Eotaxins are cytokines that promote pulmonary eosinophilia via the receptor CCR3. Single-nucleotide polymorphisms (SNPs) in CCR3 and eotaxin genes are associated with asthma. In this study, genetic interactions among SNPs of several eotaxin genes and CCR3 were assessed and their relationship with blood eosinophilia in asthma was examined. METHODS: A total of 533 asthmatics were enrolled in this study. Asthmatics with eosinophilia (>0.5x109/L) were compared with those without eosinophilia (A (29L>I) was significantly associated with 3 of the 4 CCR3 SNPs among asthmatics with eosinophilia (P=0.037-0.009). EOT2+304C>A (29L>I) and the CCR3 SNPs were also significantly associated with blood eosinophilia in an interaction model constructed by logistic regression (P=0.0087). GMDR analysis showed that the combination of EOT2+304C>A (29L>I) and CCR3-174C>T was the best model (accuracy=0.536, P=0.005, CVC 9/10). CONCLUSIONS: The epistatic influence of CCR3 on eotaxin gene variants indicates that these variants may be candidate markers for eosinophilia in asthma.

Gene - Gene Interactions Among MCP Genes Polymorphisms in Asthma

PURPOSE: Monocyte chemoattractant proteins (MCPs) are important cytokines that involved in cellular activation and releasing of inflammatoy mediators by basophils and eosinophils in allergic disease. Some MCP gene variants implicate in asthma and monoclonal antibody for MCP-3 blocks allergic inflammations in the patients with asthma. Detection of interactions between gene and environment or between genes for complex disease such as asthma is important. We searched for an evidence of genetic effect of single nucleotide polymorphisms (SNPs) of MCP genes as well as gene - gene interactions involved in asthma. METHODS: Four hundreds asthmatics and four hundreds normal controls were enrolled. Asthma was defined as a positive bronchodilator response or positive methacholine provocation test with compatible clinical symptoms. Seven MCP gene SNPs (2 SNPs in MCP-1, 1 in MCP-2, and 4 in MCP-3) were included. Association analyses between SNP and asthma, and the tests for gene - gene interaction were performed. RESULTS: Strong linkage disequilibria were found among 7 MCP gene polymorphisms. There was no SNP that showed a significant association with asthma among 7 SNPs of 3 MCP genes. No haplotype was associated with asthma, either. The combination of MCP1-2518G>A, MCP2+46A>C, and MCP3+563C>T was the best predictive model for asthma as compared to the control in tests for gene - gene interaction. The MCP1-2518G>A and MCP2+46A>C was the second best predictive combination and this had the highest synergistic interaction effect on the subject's status than any other combination of polymorphisms. Complete linkages were not associated with the gene - gene interactions models. CONCLUSIONS: MCP gene polymorphisms probably interact with each other; thus, these findings may help in developing a possible genetic marker to predict asthma.

Gene - Gene Interactions Among MCP Genes Polymorphisms in Asthma

PURPOSE: Monocyte chemoattractant proteins (MCPs) are important cytokines that involved in cellular activation and releasing of inflammatoy mediators by basophils and eosinophils in allergic disease. Some MCP gene variants implicate in asthma and monoclonal antibody for MCP-3 blocks allergic inflammations in the patients with asthma. Detection of interactions between gene and environment or between genes for complex disease such as asthma is important. We searched for an evidence of genetic effect of single nucleotide polymorphisms (SNPs) of MCP genes as well as gene - gene interactions involved in asthma. METHODS: Four hundreds asthmatics and four hundreds normal controls were enrolled. Asthma was defined as a positive bronchodilator response or positive methacholine provocation test with compatible clinical symptoms. Seven MCP gene SNPs (2 SNPs in MCP-1, 1 in MCP-2, and 4 in MCP-3) were included. Association analyses between SNP and asthma, and the tests for gene - gene interaction were performed. RESULTS: Strong linkage disequilibria were found among 7 MCP gene polymorphisms. There was no SNP that showed a significant association with asthma among 7 SNPs of 3 MCP genes. No haplotype was associated with asthma, either. The combination of MCP1-2518G>A, MCP2+46A>C, and MCP3+563C>T was the best predictive model for asthma as compared to the control in tests for gene - gene interaction. The MCP1-2518G>A and MCP2+46A>C was the second best predictive combination and this had the highest synergistic interaction effect on the subject's status than any other combination of polymorphisms. Complete linkages were not associated with the gene - gene interactions models. CONCLUSIONS: MCP gene polymorphisms probably interact with each other; thus, these findings may help in developing a possible genetic marker to predict asthma.

Acute eosinophilic pneumonia related to a mesalazine suppository

It has been well known that mesalazine can cause the interstitial lung disease, such as Bronchiolitis obliterans with organizing pneumonia (BOOP), Non-Specific Interstitial Pneumonia (NSIP), or eosinophilic pneumonia. 5-Aminosalicylic acid (5-ASA), mesalazine, and sulfasalazine are important drugs for treating inflammatory bowel disease. Topical products of these limited systemic absorption and have less frequent side effects, therefore suppository form of these drugs have been used more than systemic drug. Most cases of measalzine-induced lung toxicity develop from systemic use of the drug. A 30-year-old woman had an interstitial lung disease after using mesalazine suppository because of ulcerative colitis. The lung biopsy demonstrated eosinophilic pneumonia combined with BOOP. She was recovered after stopping of mesalazine suppository and treatment with systemic steroid.

The differences of clinical profiles by house dust mite sensitization in patients with asthmatics in Soonchunhyang University Hospital cohort

PURPOSE: The majority of patients with allergic disease are highly sensitized to house dust mites (HDM). There is few data to observe sensitization rate to HDM in asthmatics in Korea. The aim of this study was to observe the differences of clinical profiles by HDM sensitization in patients with asthmatics in Soonchunhyang University Hospital (SCH) cohort. METHODS: We recruited 2,345 asthmatic patients in SCH cohort. Lung function, body mass index and sputum and blood eosinophils, and PC20, and clinical profiles were compared by HDM sensitization. RESULTS: Dermatophagoides farinae (Derf) and/or Dermatophagoides pteronyssinus (Derp) (+) sensitization rate was higher prevalence in male than in female. Compared with nonatopy asthmatics, Derf and/or Derp (+) asthmatics had early onset of age [Derf and/or Derp (+) vs. Derf and Derp (-) vs. atopy (-); 32.5+/-0.51 vs. 36.1+/-0.88 vs. 43.1+/-0.54, P<0.05]. Derf and/or Derp (+) asthmatics had shorter duration of asthma symptom than that of nonatopy asthmatics. Derf and/or Derp (+) asthmatics had lower forced expiratory volume in one second and forced vital capacity than those of Derf and Derp (-) asthmatics. PC20 in Derf and/or Derp (+) asthmatics had lower than those of Derf and Derp (-) and nonatopy asthmatics [Derf and/or Derp (+) vs. Derf and Derp (-) vs. atopy (-); 5.4+/-0.24 mg/mL vs. 6.59+/-0.52 mg/mL vs. 7.19+/-0.33 mg/mL, P<0.05]. Blood eosinophils number in Derf and/or Derp (+) asthmatics had higher than that of nonatopy asthmatics (414.7+/-131.1 vs. 350.6+/-14.0, P<0.05). Total immunoglobulin E (IgE) in Derf and/or Derp positive asthmatics had higher than that of Derf and Derp negative and nonatopy asthmatics. There was no difference of body mass index among three groups. CONCLUSIONS: Our data indicate that atopy asthmatics sensitized to Derf and/or Derp had early onset of age, high total IgE and airway responsiveness, and eosinophilic inflammation.

A Case of Skin Sclerosis Associated with Docetaxel Chemotherapy for Non-Small Cell Lung Cancer

A 64-year-old woman was diagnosed with non-small cell lung cancer. Her disease was stage 4 (T2N2M1) with squamous cell carcinoma. She had been treated with docetaxel and carboplatin. After a completion of 11 cycle of chemotherapy, edema appeared on both feet and had spread rapidly up to the pretibial area without response to diuretics. Sclerotic changes and pigmentation followed but both knees and other parts of the body were spared. There was no evidence of vascular occlusions. On serologic tests, antinuclear, anti-centromere, and anti-topoisomerase I antibodies were all negative. A skin biopsy revealed diffuse infiltration of lymphocytes and discretely thickened collagen bundles in the superficial dermis. After discontinuing docetaxel chemotherapy, she was treated with prednisolone and D-penicillamine and sclerotic changes on the lower legs were improved.

A Case of Propofol-Induced Oropharyngeal Angioedema and Bronchospasm

Propofol (2,6-diisopropylphenol) is an ultrashort-acting sedative agent with sedative and amnestic effects that is used not only for anesthesia but also for sedation during minor outpatient procedures and endoscopic examinations. Rare cases of anaphylaxis following propofol administration have been reported in the medical literature. Documentation of anaphylaxis is often lacking because the cause and effect relationship is often hard to prove. Only a minority of patients get referred for allergy testing to confirm the offending drug. Here we report a 74-year-old woman who had an anaphylactic reaction with severe oropharyngeal edema and bronchospasm for a few minutes after receiving propofol during endoscopic examination. An allergy skin test was positive for both propofol and soybean. Soybean in the intralipid is one component of propofol, and we concluded that this anaphylaxis was caused by soybean.

Novel Drugs for Asthma Treatment: Immunomodulatory Therapy / 대한내과학회지

The management of asthma focuses on the reduction of airway inflammation accompany with symptomatic care after recognition. Glucocorticosteroid is the most important drug to reduce airway inflammation, and it has been used inhaled, orally and systemically. New knowledge about the pathogenesis of allergy and asthma has made the development and clinical trial of target or immunomodulator therapy. It includes cytokine, cytokine blockers, specific cytokine receptor blocker, and immunostimulatory oligodeoxynucleotides. These agents are thought to hold the promise for more beneficial outcomes in the future, although it showed limited therapeutic benefits only for patients, especially intractable or severe asthma, until now.

Evaluating a Thrombosed Azygous Vein Aneurysm Combined with Pulmonary Arterial Thromboembolism by ECG-Gated Multidetector CT: a Case Report

Azygous vein aneurysm is a rare congenital lesion that needs to be differentiated from mediastinal mass lesions. Although almost of these anomalies are asymptomatic lesions, we experienced an interesting case in which a thrombus within an azygous vein aneurysm in a 75-year-old woman caused pulmonary thromboembolism. The patient was managed by medical treatment for one month and then the thrombus within both the azygous vein aneurysm and the pulmonary arteries completely resolved.

A Case of Pulmonary Siderosis Mimicking Metastatic Lung Cancer / 결핵및호흡기질환

Pulmonary siderosis is a pneumoconiosis caused by chronic iron inhalation. A diagnosis of pulmonary siderosis is based on a patient history of iron inhalation, on chest radiographic findings, and on accumulation of iron oxide in macrophages within the lung. A typical radiographic finding of pulmonary siderosis includes ill-defined micronodules that are diffusely distributed in the lung. We experienced a 52-year-woman with a 1.3x1.5-cm mass in the left upper lobe with multiple nodules in both lungs. Because the radiographic findings were atypical, we conducted a video-assisted thorascopic lung biopsy procedure to exclude the diagnosis of metastatic lung cancer. After confirming iron deposition in the lung tissue and knowing the patient's occupational history of welding iron, we concluded that this was a case of pulmonary siderosis.

A Case of Pulmonary Siderosis Mimicking Metastatic Lung Cancer / 결핵및호흡기질환

Pulmonary siderosis is a pneumoconiosis caused by chronic iron inhalation. A diagnosis of pulmonary siderosis is based on a patient history of iron inhalation, on chest radiographic findings, and on accumulation of iron oxide in macrophages within the lung. A typical radiographic finding of pulmonary siderosis includes ill-defined micronodules that are diffusely distributed in the lung. We experienced a 52-year-woman with a 1.3x1.5-cm mass in the left upper lobe with multiple nodules in both lungs. Because the radiographic findings were atypical, we conducted a video-assisted thorascopic lung biopsy procedure to exclude the diagnosis of metastatic lung cancer. After confirming iron deposition in the lung tissue and knowing the patient's occupational history of welding iron, we concluded that this was a case of pulmonary siderosis.

Asthmatics Without Rhinitis Have More Fixed Airway Obstruction Than Those With Concurrent Rhinitis

PURPOSE: Rhinitis and asthma usually occur together. There are increasing evidences that allergic rhinitis (AR) may influence the clinical course of asthma. The aim of this study is to evaluate clinical parameters and therapeutic response in patients with between asthma and asthma with AR. METHODS: Four-hundred eighty-five patients with asthma and 428 asthmatics with AR, who had lesser than 50 years old and smoked less than 10 pack-years were recruited. We compared FEV1 and FEV1/FVC following bronchodilator, atopy, IgE, emphysema on HRCT, and aspirin intolerance between two groups. Also we compared physiologic fixed airway obstruction defined using FEV1/FVC and FEV1 less than 75% following anti-asthmatic drug for 1 year. RESULTS: 46.8% (428/913) asthmatics suffered from AR. There were no differences of total IgE, body mass index, PC20, sputum eosinophils and emphysema on HRCT between two groups. The age in asthmatics was higher than that in those with AR. FEV1/FVC was lower in asthmatics than in those with AR. The prevalence of atopy was higher in asthmatics with AR than in asthmatics. Aspirin intolerance was higher in asthmatics with AR than in asthmatics (42/218 vs 13/109, P=0.001). Fixed airway obstruction were more observed in asthmatics than in those with AR (39/319 vs 28/355, P=0.001) after anti-asthmatic drug for 1 year. CONCLUSIONS: Asthmatics with AR had more atopy and aspirin intolerance than asthmatics, and asthmatics had poor response to anti-inflammatory drugs than those with concurrent rhinitis, indicating that asthmatics have more fixed airway obstruction than those with concurrent rhinitis.

Asthmatics Without Rhinitis Have More Fixed Airway Obstruction Than Those With Concurrent Rhinitis

PURPOSE: Rhinitis and asthma usually occur together. There are increasing evidences that allergic rhinitis (AR) may influence the clinical course of asthma. The aim of this study is to evaluate clinical parameters and therapeutic response in patients with between asthma and asthma with AR. METHODS: Four-hundred eighty-five patients with asthma and 428 asthmatics with AR, who had lesser than 50 years old and smoked less than 10 pack-years were recruited. We compared FEV1 and FEV1/FVC following bronchodilator, atopy, IgE, emphysema on HRCT, and aspirin intolerance between two groups. Also we compared physiologic fixed airway obstruction defined using FEV1/FVC and FEV1 less than 75% following anti-asthmatic drug for 1 year. RESULTS: 46.8% (428/913) asthmatics suffered from AR. There were no differences of total IgE, body mass index, PC20, sputum eosinophils and emphysema on HRCT between two groups. The age in asthmatics was higher than that in those with AR. FEV1/FVC was lower in asthmatics than in those with AR. The prevalence of atopy was higher in asthmatics with AR than in asthmatics. Aspirin intolerance was higher in asthmatics with AR than in asthmatics (42/218 vs 13/109, P=0.001). Fixed airway obstruction were more observed in asthmatics than in those with AR (39/319 vs 28/355, P=0.001) after anti-asthmatic drug for 1 year. CONCLUSIONS: Asthmatics with AR had more atopy and aspirin intolerance than asthmatics, and asthmatics had poor response to anti-inflammatory drugs than those with concurrent rhinitis, indicating that asthmatics have more fixed airway obstruction than those with concurrent rhinitis.

The Impact of Smoking on Clinical and Therapeutic Effects in Asthmatics

Smoking is associated with poor symptom control and impaired therapeutic responses in asthma. A total of 843 patients with asthma were recruited. The patients received treatment for 1 yr according to the severity of their asthma. We compared the forced expiratory volume in 1 sec (FEV1), the ratio of FEV1 to forced vital capaity (FVC), atopy, total IgE, emphysema on high-resolution computed tomography (HRCT), the number of near-fatal asthma attacks, and physiological fixed airway obstruction between the smoking and nonsmoking groups. The study population consisted of 159 (18.8%) current smokers, 157 (18.7%) ex-smokers, and 525 (62.5%) nonsmokers. Although the prevalence of atopy was not different between the smoking and nonsmoking groups, the total IgE was higher among the smokers than the nonsmokers. Compared with the nonsmoking group, the smokers had a lower FEV1 % predicted and forced expiratory flow between 25 and 75% of FVC. A greater prevalence of emphysema and a significantly higher number of asthmatic patients with fixed airway obstruction were detected in the smoking versus nonsmoking group. The 37.5% of asthmatic patients who were former or current smokers showed decreased pulmonary function and increased IgE, emphysema on HRCT, and fixed airway obstruction, indicating that smoking can modulate the clinical and therapeutic responses in asthma.

A Case of Goodpasture's Syndrome in a Foundry Worker / 대한산업의학회지

BACKGROUND: Smoking, upper respiratory tract infection, genetic factors and hydrocarbons are known as risk factors of Goodpasture's syndrome. We studied a patient with Goodpasture's syndrome who had worked for 27 years in a foundry company. Based on a study on the work-relatedness of the syndrome, we describe and discuss our study results. CASE: A 46-year-old man, who had worked as a foundry worker for 27 years and had a 12 1/2 packyear history of smoking cigarettes, was admitted into a hospital on 15th February 2006 with coughing, chest pain and dyspnea. On admission, he had hematuria, proteinuria, severe restrictive pulmonary function disorder and rapid elevation of blood urea nitrogen/creatinine. Immunological examination showed ANA (+), ANCA (-) and Anti-GBM Ab (+). Kidney biopsy showed pauci-immune crescentic glomerulonephritis. Mild bleeding was revealed through bronchoscopy and no vasculitis and granuloma were present on at lung biopsy. Finally, we diagnosed the worker's illness as Goodpasture's syndrome and carried out hemodialysis and plasmapheresis. In the workplace survey, the exposure level of respirable crystalline silica exceeded the TLV-TWA (0.0106 mg/m3), which was calibrated for overtime. CONCLUSION: Based on both the clinical test and industrial hygiene examination, we concluded that the Goodpasture's syndrome in this case was caused by long-term silica exposure.

A Case of Goodpasture's Syndrome in a Foundry Worker / 대한산업의학회지

BACKGROUND: Smoking, upper respiratory tract infection, genetic factors and hydrocarbons are known as risk factors of Goodpasture's syndrome. We studied a patient with Goodpasture's syndrome who had worked for 27 years in a foundry company. Based on a study on the work-relatedness of the syndrome, we describe and discuss our study results. CASE: A 46-year-old man, who had worked as a foundry worker for 27 years and had a 12 1/2 packyear history of smoking cigarettes, was admitted into a hospital on 15th February 2006 with coughing, chest pain and dyspnea. On admission, he had hematuria, proteinuria, severe restrictive pulmonary function disorder and rapid elevation of blood urea nitrogen/creatinine. Immunological examination showed ANA (+), ANCA (-) and Anti-GBM Ab (+). Kidney biopsy showed pauci-immune crescentic glomerulonephritis. Mild bleeding was revealed through bronchoscopy and no vasculitis and granuloma were present on at lung biopsy. Finally, we diagnosed the worker's illness as Goodpasture's syndrome and carried out hemodialysis and plasmapheresis. In the workplace survey, the exposure level of respirable crystalline silica exceeded the TLV-TWA (0.0106 mg/m3), which was calibrated for overtime. CONCLUSION: Based on both the clinical test and industrial hygiene examination, we concluded that the Goodpasture's syndrome in this case was caused by long-term silica exposure.

Impact of Circulating TGF-beta and IL-10 on T Cell Cytokines in Patients with Asthma and Tuberculosis

Regulatory T cells, which stimulate or inhibit the effector functions of distinct T cell subsets, are critical in the control of the immune response. We investigated the effect of TGF-beta and IL-10 on T cell subsets according to the Th1/Th2 immune status. Sixty-two patients with asthma and 38 patients with pulmonary tuberculosis were included. Allergy skin tests, tuberculin tests, and chest radiography were performed. The levels of circulating IL-4, IFN-gamma, TGF-beta1, and IL-10 were measured using ELISA. The level of TGF-beta1 was higher in patients with asthma than in those with tuberculosis, but the IL-10 levels were the same between the asthma and tuberculosis groups. Atopy was unrelated to the tuberculin response. The IFN-gamma level was correlated with the IL-10 level, and the level of IL-4 was unrelated to the IL-10 or TGF-beta1 level. The level of IL-10 was higher in the negative tuberculin reactors than in the positive tuberculin reactors among patients with asthma, and TGF-beta1 was higher in the positive tuberculin reactors than in the negative tuberculin reactors among patients with tuberculosis. These results demonstrate that the regulatory effects of circulating TGF-beta and IL-10 on T cell cytokines may be different between Th2-type asthma and Th1 tuberculosis.

Aquaporin in bleomycin induced lung injury / 결핵및호흡기질환

BACKGROUND: Aquaporins (AQPs) may play a role in the pathogenesis of pulmonary inflammation and edema. This study investigated the role ofAQPs in acute lung injury following bleomycin inhalation in rats. METHODS: Sprague-Dawley rats were treated via inhalation with 10 U/kg bleomycin hydrochloride dissolved in 5 ml of normal saline. The control rats were treated with 5 ml normal saline. The animals (n = 6-8 rats per group) were sacrificed at 4, 7, and 14 d. The changes in AQP1, AQP4, and AQP5 expression levels over time were analyzed by Western blotting. The nitrate and nitrite concentrations in the bronchoalveolar lavage fluid (BALF) were measured using a modified Griess reaction. ELISA was used to check cytokines. RESULTS: The respiration rates were significantly higher 4 and 7 days after the bleomycin treatment compared with those of the control rats. The tidal volume was lower in rats at 4 days after the bleomycin treatment, and the wet/dry weights of the lung were significantly higher than those of the control group. The nitrite and nitrate concentrations in the BALF from the rats at 4 days after exposure to bleomycin were greater than those from the saline-treated rats. Immunoblotting studies demonstrated that the AQP1 and AQP4 expression levels were lower in the rats at 4 days. However, the AQP4 expression level was higher at 7 days. The AQP5 expression level increased at 4, 7 and 14 days after the bleomycin treatment. CONCLUSION: This study demonstrates that AQPs are expressed differently in bleomycin-induced pulmonary edema.