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1. Full Text Macrophage-epithelial paracrine crosstalk inhibits lung edema clearance during influenza infection
by Peteranderl, Christin and Morales-Nebreda, Luisa and Selvakumar, Balachandar and Lecuona, Emilia and Vadász, István and Morty, Rory E and Schmoldt, Carole and Bespalowa, Julia and Wolff, Thorsten and Pleschka, Stephan and Mayer, Konstantin and Gattenloehner, Stefan and Fink, Ludger and Lohmeyer, Juergen and Seeger, Werner and Sznajder, Jacob I and Mutlu, Gökhan M and Budinger, G. R. Scott and Herold, Susanne
Journal of Clinical Investigation, ISSN 0021-9738, 04/2016, Volume 126, Issue 4, pp. 1566 - 1580
Influenza A viruses (IAV) can cause lung injury and acute respiratory distress syndrome (ARDS), which is characterized by accumulation of excessive fluid... 
MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | ACTIVATED PROTEIN-KINASE | APOPTOSIS-INDUCING LIGAND | VIRUS-INFECTION | CYTOKINE RESPONSES | IN-VIVO | ALVEOLAR FLUID CLEARANCE | LIQUID CLEARANCE | UP-REGULATION | RESPIRATORY-DISTRESS-SYNDROME | Respiratory Distress Syndrome, Adult - pathology | Macrophages, Alveolar - pathology | Pulmonary Alveoli - pathology | Humans | Orthomyxoviridae Infections - pathology | TNF-Related Apoptosis-Inducing Ligand - immunology | Interferon Type I - immunology | Paracrine Communication - immunology | Respiratory Mucosa - pathology | Respiratory Distress Syndrome, Adult - immunology | Animals | Respiratory Mucosa - immunology | Pulmonary Edema - immunology | Influenza A virus - immunology | Pulmonary Edema - pathology | Mice | Sodium-Potassium-Exchanging ATPase - immunology | Macrophages, Alveolar - immunology | Orthomyxoviridae Infections - immunology | Lung diseases | Influenza | Physiological aspects | Development and progression | Genetic aspects | Properties | Adenosine triphosphatase | Proteins | Flow cytometry | Edema | Sodium | Respiratory distress syndrome | Rodents | Infections | Communications networks | Gene expression
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2. Full Text Mast cells contribute to Enterovirus 71 infection-induced pulmonary edema in neonatal mice
by Jin, Yuefei and Zhang, Chao and Wang, Hui and Zhou, Guangyuan and Wang, Xiangpeng and Zhang, Rongguang and Chen, Shuaiyin and Ren, Jingchao and Chen, Lu and Dang, Dejian and Zhang, Peng and Xi, Yuanlin and Wu, Weidong and Zhang, Weiguo and Duan, Guangcai
Laboratory Investigation, ISSN 0023-6837, 08/2018, Volume 98, Issue 8, pp. 1039 - 1051
Enterovirus (EV) 71 infection has been widely acknowledged as the leading cause of severe hand, foot and mouth disease (HFMD), which may rapidly lead to fatal... 
MEDICINE, RESEARCH & EXPERIMENTAL | IMMUNITY | LUNG | INFLAMMATION | DISEASE | PATHOLOGY | STRAIN | EOTAXIN | Enterovirus Infections - metabolism | Humans | Mast Cells - virology | Brain - virology | Muscle, Skeletal - metabolism | Vascular Endothelial Growth Factor A - metabolism | Histamine - immunology | Brain - metabolism | Histamine - metabolism | Lung - virology | Enterovirus Infections - virology | Muscle, Skeletal - immunology | Enterovirus Infections - immunology | Mast Cells - metabolism | Lung - metabolism | Muscle, Skeletal - virology | Pulmonary Edema - metabolism | Cytokines - immunology | Disease Models, Animal | Animals, Newborn | Mast Cells - immunology | Pulmonary Edema - virology | Cytokines - metabolism | Enterovirus A, Human - immunology | Enterovirus A, Human - physiology | Vascular Endothelial Growth Factor A - immunology | Animals | Pulmonary Edema - immunology | Mice, Inbred BALB C | Brain - immunology | Lung - immunology | Neonates | Platelet-activating factor | Interleukin | Infections | Lymphocytes T | Hand-foot-and-mouth disease | Interleukin 5 | Lymphocytes | Tumor necrosis factor-TNF | Vascular endothelial growth factor | Noradrenaline | Growth factors | Edema | Foot and mouth disease | Dendritic cells | Leukocytes (eosinophilic) | Hypersensitivity | Organs | Muscles | Interleukin 13 | Inflammation | Tumor necrosis factor-α | Skeletal muscle | Histamine | Monocytes | Lungs | Nitric oxide | Tryptase | Endocrine glands | Mice | Norepinephrine | Foot-and-mouth disease | Mast cells | Eosinophils
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3. Full Text Influenza leaves a TRAIL to pulmonary edema
by Brauer, Rena and Chen, Peter
Journal of Clinical Investigation, ISSN 0021-9738, 04/2016, Volume 126, Issue 4, pp. 1245 - 1247
Influenza infection can cause acute respiratory distress syndrome (ARDS), leading to poor disease outcome with high mortality. One of the driving features in... 
CONTROLLED CLINICAL-TRIAL | MEDICINE, RESEARCH & EXPERIMENTAL | CLEARANCE | VIRUS | EPITHELIAL-CELLS | NA,K-ATPASE | INFLAMMATION | ACUTE LUNG INJURY | FLUID TRANSPORT | ENDOCYTOSIS | RESPIRATORY-DISTRESS-SYNDROME | Animals | Humans | Respiratory Mucosa - immunology | Pulmonary Edema - immunology | Influenza A virus - immunology | TNF-Related Apoptosis-Inducing Ligand - immunology | Interferon Type I - immunology | Paracrine Communication - immunology | Macrophages, Alveolar - immunology | Orthomyxoviridae Infections - immunology | Development and progression | Genetic aspects | Interferon | Cytokines | Properties | Influenza | Sodium | Kinases | Mortality | Rodents | Apoptosis
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4. Full Text TNF-induced death signaling triggers alveolar epithelial dysfunction in acute lung injury
by Patel, Brijesh V and Wilson, Michael R and O'Dea, Kieran P and Takata, Masao
Journal of Immunology, ISSN 0022-1767, 04/2013, Volume 190, Issue 8, pp. 4274 - 4282
The ability of the alveolar epithelium to prevent and resolve pulmonary edema is a crucial determinant of morbidity and mortality in acute lung injury (ALI).... 
APOPTOSIS | TUMOR-NECROSIS-FACTOR | ENDOTHELIAL-CELLS | ANIMAL-MODELS | VIVO MOUSE MODEL | IMMUNOLOGY | FLUID CLEARANCE | PULMONARY-EDEMA | RESPIRATORY-DISTRESS-SYNDROME | SOLUBLE FAS LIGAND | FACTOR-ALPHA | Tumor Necrosis Factor-alpha - metabolism | Macrophages, Alveolar - pathology | Caspase 8 - toxicity | Mice, Inbred C57BL | Cell Death - immunology | Inflammation Mediators - toxicity | Male | Receptors, Tumor Necrosis Factor, Type I - genetics | Tumor Necrosis Factor-alpha - toxicity | Acute Lung Injury - pathology | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type I - deficiency | Signal Transduction - immunology | Animals | Inflammation Mediators - metabolism | Pulmonary Edema - immunology | Acute Lung Injury - immunology | Pulmonary Edema - pathology | Acute Lung Injury - metabolism | Mice | Macrophages, Alveolar - metabolism | Pulmonary Edema - metabolism | Receptors, Tumor Necrosis Factor, Type I - toxicity | Macrophages, Alveolar - immunology | Pulmonary Edema | Death Domain Receptors | TNFRSF1A Receptor | ARDS | Apoptosis
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5. Full Text Pathogenesis of High-Altitude Pulmonary Edema: Inflammation Is Not an Etiologic Factor
by Swenson, Erik R and Maggiorini, Marco and Mongovin, Stephen and Gibbs, J. Simon R and Greve, Ilona and Mairbäurl, Heimo and Bärtsch, Peter
JAMA, ISSN 0098-7484, 05/2002, Volume 287, Issue 17, pp. 2228 - 2235
CONTEXT The pathogenesis of high-altitude pulmonary edema (HAPE) is considered an altered permeability of the alveolar-capillary barrier secondary to intense... 
STRESS FAILURE | LUNG | MEDICINE, GENERAL & INTERNAL | PERMEABILITY | FLUID | REDISTRIBUTION | RABBIT | HYPOXIA | ACUTE MOUNTAIN-SICKNESS | INHALED NITRIC-OXIDE | BRONCHOALVEOLAR LAVAGE | Blood Pressure | Humans | Middle Aged | Bronchoalveolar Lavage Fluid - immunology | Male | Hemorrhage | Pulmonary Edema - etiology | Altitude Sickness - immunology | Adult | Female | Leukocyte Count | Bronchoscopy | Echocardiography | Cytokines - metabolism | Blood Gas Analysis | Pulmonary Edema - diagnostic imaging | Inflammation | Pulmonary Artery - physiology | Radiography | Eicosanoids - metabolism | Pulmonary Edema - immunology | Altitude Sickness - complications | Bronchoalveolar Lavage Fluid - chemistry | Erythrocyte Count | Altitude | Serum Albumin - metabolism | Causes of | Mountain sickness | Physiological aspects | Pulmonary edema | Pathology | Altitudes | Blood pressure | Medical disorders | Coronary vessels
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6. Full Text Pathogenesis of Enterovirus 71 Brainstem Encephalitis in Pediatric Patients: Roles of Cytokines and Cellular Immune Activation in Patients with Pulmonary Edema
by Shih-Min Wang and Huan-Yao Lei and Kao-Jean Huang and Jing-Ming Wu and Jen-Ren Wang and Chun-Keung Yu and Ih-Jen Su and Ching-Chuan Liu
The Journal of Infectious Diseases, ISSN 0022-1899, 8/2003, Volume 188, Issue 4, pp. 564 - 570
Taiwan experienced several epidemics of enterovirus 71 (EV71) infections, which were associated with brainstem encephalitis (BE) and pulmonary edema (PE). To... 
T lymphocytes | Cytokines | Lymphocytes | Brain stem | Pathogenesis | Mouth diseases | Viruses | Enterovirus | Infections | Natural killer cells | Pulmonary edema | RESPONSES | INFECTIOUS DISEASES | TAIWAN | DISEASE | INJURY | CENTRAL-NERVOUS-SYSTEM | INFECTION | INTERLEUKIN-10 | IL-10 | CHILDREN | MANIFESTATIONS | Encephalitis, Viral - virology | Humans | Child, Preschool | Infant | Male | Encephalitis, Viral - complications | Interleukins - metabolism | CD4-Positive T-Lymphocytes - immunology | Leukocytes - immunology | Brain Stem - pathology | Enterovirus Infections - complications | Enterovirus Infections - immunology | Pulmonary Edema - complications | Killer Cells, Natural - immunology | Female | Cytokines - immunology | Cytokines - metabolism | CD4 Lymphocyte Count | Enterovirus - isolation & purification | Brain Stem - virology | Pulmonary Edema - immunology | Brain Stem - immunology | Encephalitis, Viral - pathology | Enterovirus Infections - pathology | CD8-Positive T-Lymphocytes - immunology | Encephalitis, Viral - immunology | Leukocytes - metabolism | Encephalitis | Care and treatment | Pathogenic microorganisms | Demographic aspects | Research | Patients | Prevention | Interleukins | Physiological aspects | Causes of | Airborne infection | Health aspects | Enterovirus diseases
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7. Full Text Improved IL-2 immunotherapy by selective stimulation of IL-2 receptors on lymphocytes and endothelial cells
by Carsten Krieg and Sven Létourneau and Giuseppe Pantaleo and Onur Boyman and James P. Allison
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2010, Volume 107, Issue 26, pp. 11906 - 11911
IL-2 immunotherapy is an attractive treatment option for certain metastatic cancers. However, administration of IL-2 to patients can lead, by ill-defined... 
Receptors | Lungs | Cell lines | Melanoma | Cellular immunity | Mice | Natural killer cells | Pulmonary edema | Endothelial cells | Tumors | Tumor | T cell | Cytokine/mAb complexes | Cytokine | NK cell | cytokine | IMMUNE-COMPLEXES | MULTIDISCIPLINARY SCIENCES | ANTIBODY | ALPHA | TOXICITY | RENAL-CANCER | tumor | cytokine/mAb complexes | IN-VIVO | BIOLOGICAL-ACTIVITY | REGULATORY T-CELLS | HIGH-DOSE INTERLEUKIN-2 | CD8(+) CELLS | Recombinant Proteins - therapeutic use | Immunotherapy - methods | Interleukin-2 - adverse effects | Homeodomain Proteins - metabolism | Humans | Interleukin-2 - therapeutic use | Interleukin-2 - antagonists & inhibitors | Recombinant Proteins - adverse effects | Lung - cytology | Pulmonary Edema - etiology | Interleukin-2 Receptor alpha Subunit - genetics | Lymphocytes - immunology | Melanoma, Experimental - immunology | Lung Neoplasms - secondary | Interleukin-2 - administration & dosage | Melanoma, Experimental - secondary | Antibodies, Monoclonal - immunology | Interleukin-2 Receptor alpha Subunit - deficiency | Melanoma, Experimental - therapy | Mice, Inbred C57BL | Receptors, Interleukin-2 - metabolism | Lung Neoplasms - therapy | Homeodomain Proteins - genetics | Recombinant Proteins - administration & dosage | Immunotherapy - adverse effects | Mice, Knockout | Endothelial Cells - immunology | Lung Neoplasms - immunology | Animals | Interleukin-2 Receptor alpha Subunit - metabolism | Antibodies, Monoclonal - administration & dosage | Pulmonary Edema - immunology | Antigen-Antibody Complex - administration & dosage | Antigen-Antibody Complex - immunology | Lung - immunology | Care and treatment | Interleukin-2 | Health aspects | Immunotherapy | Methods | Biological Sciences | mAb complexes
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8. Full Text Selective HDAC6 inhibition prevents TNF-α-induced lung endothelial cell barrier disruption and endotoxin-induced pulmonary edema
by Yu, Jinyan and Ma, Zhongsen and Shetty, Sreerama and Ma, Mengshi and Fu, Jian
American Journal of Physiology - Lung Cellular and Molecular Physiology, ISSN 1040-0605, 07/2016, Volume 311, Issue 1, pp. L39 - L47
Selective HDAC6 inhibition prevents TNF-alpha-induced lung endothelial cell barrier disruption and endotoxin-induced pulmonary edema. Am J Physiol Lung Cell... 
Tubulin | Endothelial barrier | Catenin | HDAC6 | Lung injury | PHYSIOLOGY | PERMEABILITY | ACTIN | catenin | ACETYLATION | DEACETYLASE | tubulin | endothelial barrier | MICROTUBULE CYTOSKELETON | BETA-CATENIN | LETHAL SEPTIC MODEL | lung injury | RESPIRATORY SYSTEM | IN-VIVO | VE-CADHERIN | DYSFUNCTION | Humans | Protein Multimerization | Capillary Permeability - drug effects | Endothelium, Vascular - drug effects | Male | Microtubules - metabolism | Tubulin - metabolism | Pulmonary Edema - prevention & control | Indoles - pharmacology | Acetylation | Hydroxamic Acids - pharmacology | Pulmonary Edema - metabolism | Endothelium, Vascular - immunology | Endothelial Cells - metabolism | Histone Deacetylase 6 | Mice, Inbred C57BL | Cells, Cultured | Histone Deacetylases - metabolism | Endothelial Cells - immunology | Animals | Endothelium, Vascular - metabolism | Lipopolysaccharides - pharmacology | Pulmonary Edema - immunology | Tumor Necrosis Factor-alpha - physiology | Histone Deacetylase Inhibitors - pharmacology | Protein Processing, Post-Translational | Endothelial Cells - drug effects | Index Medicus
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9. Full Text Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury
by Eickmeier, O and Seki, H and Haworth, O and Hilberath, J.N and Gao, F and Uddin, M and Croze, R.H and Carlo, T and Pfeffer, M.A and Levy, B.D
Mucosal Immunology, ISSN 1933-0219, 03/2013, Volume 6, Issue 2, pp. 256 - 266
Acute lung injury (ALI) is a severe illness with excess mortality and no specific therapy. Protective actions were recently uncovered for docosahexaenoic... 
ANTIOXIDANTS | LIPOXIN-A | NEUTROPHILS | MICE | MECHANISMS | GAMMA-LINOLENIC ACID | MEDIATORS | OUTCOMES | IMMUNOLOGY | EICOSAPENTAENOIC ACID | Male | Airway Resistance | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | Aspirin - administration & dosage | Leukocytes - immunology | Respiratory Mucosa - pathology | Inflammation - metabolism | Inflammation Mediators - metabolism | Receptors, Formyl Peptide - metabolism | Pulmonary Edema - pathology | Acute Lung Injury - metabolism | Aspirin - pharmacology | Pulmonary Edema - metabolism | Blood-Air Barrier - physiopathology | Disease Models, Animal | Neutrophils - immunology | Inflammation - immunology | Acute Lung Injury - pathology | Animals | Transcription Factor RelA - metabolism | Blood Platelets - metabolism | Anti-Inflammatory Agents, Non-Steroidal - administration & dosage | Pulmonary Edema - immunology | Mice | Macrophages, Alveolar - metabolism | Respiratory Mucosa - metabolism | Adaptor Proteins, Signal Transducing - metabolism | Docosahexaenoic Acids - biosynthesis | Epinephrine - metabolism | Docosahexaenoic Acids - metabolism
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10. Full Text The pathogenesis of transfusion-related acute lung injury (TRALI)
by Bux, Jurgen and Sachs, Ulrich J. H
British Journal of Haematology, ISSN 0007-1048, 03/2007, Volume 136, Issue 6, pp. 788 - 799
Summary In recent years, transfusion-related acute lung injury (TRALI) has developed from an almost unknown transfusion reaction to the most common cause of... 
granulocytes | transfusion | transfusion-related acute lung injury | neutrophils | transfusion‐related acute lung injury | Transfusion | Granulocytes | Transfusion-related acute lung injury | Neutrophils | BACTERIAL LIPOPOLYSACCHARIDE | COLONY-STIMULATING FACTOR | TRANSENDOTHELIAL MIGRATION | RESPIRATORY-DISTRESS-SYNDROME | HUMAN-NEUTROPHILS | RED-BLOOD-CELLS | PLATELET-ACTIVATING-FACTOR | OF-THE-LITERATURE | HEMATOLOGY | CLASS-II ANTIBODIES | POLYMORPHONUCLEAR NEUTROPHILS | Humans | Neutrophils - immunology | Blood Component Transfusion - adverse effects | Hypoxia - complications | Neutrophil Infiltration | Pulmonary Edema - etiology | Respiratory Distress Syndrome, Adult - etiology | Syndrome | Transfusion Reaction | Isoantibodies - blood | Respiratory Distress Syndrome, Adult - immunology | Isoantigens - immunology | Pulmonary Edema - immunology | Antibodies - blood | Transplantation Immunology | Lung - blood supply
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11. Full Text VCAM-1-mediated neutrophil infiltration exacerbates ambient fine particle-induced lung injury
by Cui, Anfeng and Xiang, Meng and Xu, Ming and Lu, Meng and Lu, Peng and Wang, Shun and Zou, Yajuan and Qiao, Ke and Jin, Chengyu and Li, Yijun and Chen, Sifeng and Chen, Alex. F
Toxicology Letters, ISSN 0378-4274, 03/2019, Volume 302, pp. 60 - 74
Fine ambient particle matter (PM2.5), a component of air pollution, is linked to inflammatory lung injury. PM2.5-induced diffuse intra-alveolar edema in the... 
Fine ambient particle matter | Vascular cell adhesion molecule-1 | Lung injury | Polymorphonuclear leukocyte | MORTALITY | INHALATION | TOXICITY | INTRATRACHEAL INSTILLATION | VCAM-1 | INFLAMMATION | Vascular cell adhesion molecule-1 | DISEASE | PARTICULATE AIR-POLLUTION | TOXICOLOGY | URBAN PM2.5 | EXPOSURE | Lung Injury - pathology | Capillary Permeability | Human Umbilical Vein Endothelial Cells - metabolism | Neutropenia - metabolism | Humans | Middle Aged | Human Umbilical Vein Endothelial Cells - immunology | Male | Neutrophil Infiltration | Alveolar Epithelial Cells - immunology | Young Adult | Alveolar Epithelial Cells - pathology | Lung Injury - metabolism | Aged, 80 and over | Neutropenia - pathology | Adult | Female | Pulmonary Edema - pathology | Lung - metabolism | Retrospective Studies | Neutrophils - metabolism | Pulmonary Edema - metabolism | Cytokines - immunology | Disease Models, Animal | Neutropenia - immunology | Neutrophils - pathology | Vascular Cell Adhesion Molecule-1 - immunology | Lung - pathology | Cytokines - metabolism | Mice, Inbred C57BL | Cells, Cultured | Neutrophils - immunology | Alveolar Epithelial Cells - metabolism | Cell Adhesion | Particle Size | Pulmonary Edema - chemically induced | Animals | Adolescent | Pulmonary Edema - immunology | Human Umbilical Vein Endothelial Cells - pathology | Particulate Matter | Aged | Lung Injury - chemically induced | Vascular Cell Adhesion Molecule-1 - metabolism | Lung Injury - immunology | Lung - immunology | Index Medicus
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12. Full Text Increased monocyte turnover is associated with interstitial macrophage accumulation and pulmonary tissue damage in SIV‐infected rhesus macaques
by Cai, Yanhui and Sugimoto, Chie and Liu, David Xianhong and Midkiff, Cecily C and Alvarez, Xavier and Lackner, Andrew A and Kim, Woong‐Ki and Didier, Elizabeth S and Kuroda, Marcelo J
Journal of Leukocyte Biology, ISSN 0741-5400, 06/2015, Volume 97, Issue 6, pp. 1147 - 1153
Accumulation of IM and increased monocyte turnover during SIV infection is associated with chronic pulmonary inflammation and tissue damage during disease... 
HIV/AIDS | lung | pathogenesis | Pathogenesis | Lung | CELLS | RECEPTOR | RISK | IMMUNOLOGY | CELL BIOLOGY | HIV-INFECTION | DISEASES | ALVEOLAR MACROPHAGES | COMPLICATIONS | HEMATOLOGY | Immunohistochemistry | Macrophages, Alveolar - pathology | Lung Diseases, Interstitial - pathology | Male | Macaca mulatta | Monocytes - immunology | CD4-Positive T-Lymphocytes - pathology | Viral Load | CD4-Positive T-Lymphocytes - immunology | Lung Diseases, Interstitial - virology | Lung - virology | Simian Acquired Immunodeficiency Syndrome - virology | Pulmonary Edema - complications | Monocytes - pathology | Calcium Ionophores - pharmacology | Pulmonary Edema - pathology | Leukocyte Count | CD4-Positive T-Lymphocytes - virology | Simian Acquired Immunodeficiency Syndrome - pathology | Macrophages, Alveolar - immunology | Simian Immunodeficiency Virus - immunology | Severity of Illness Index | Macrophages, Alveolar - virology | Lung - pathology | Pulmonary Edema - virology | Lung Diseases, Interstitial - complications | Simian Acquired Immunodeficiency Syndrome - complications | Lung Diseases, Interstitial - immunology | Monocytes - virology | Animals | Simian Acquired Immunodeficiency Syndrome - immunology | Macrophages, Alveolar - drug effects | Lipopolysaccharides - pharmacology | Pulmonary Edema - immunology | Interleukin-6 - biosynthesis | CD4-Positive T-Lymphocytes - drug effects | Lung - immunology | AIDS | Host Defense & Pathophysiology | HIV
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13. Full Text The Pseudomonas aeruginosa exoenzyme Y impairs endothelial cell proliferation and vascular repair following lung injury
by Stevens, Trevor C and Ochoa, Cristhiaan D and Morrow, K. Adam and Robson, Matthew J and Prasain, Nutan and Zhou, Chun and Alvarez, Diego F and Frank, Dara W and Balczon, Ron and Stevens, Troy
American Journal of Physiology - Lung Cellular and Molecular Physiology, ISSN 1040-0605, 2014, Volume 306, Issue 10, pp. L915 - L924
Exoenzyme Y (ExoY) is a Pseudomonas aeruginosa toxin that is introduced into host cells through the type 3 secretion system (T3SS). Once inside the host cell... 
Tau | Permeability | Cyclase | Pulmonary edema | Microtubules | Pseudomonas aeruginosa - immunology | Lung - microbiology | Microvessels - physiopathology | Cell Proliferation | Microvessels - pathology | Male | Pseudomonas aeruginosa - physiology | Glucosyltransferases - physiology | Endothelial Cells - microbiology | Pseudomonas aeruginosa - enzymology | Cyclic AMP - metabolism | Pneumonia, Bacterial - pathology | Endothelial Cells - physiology | Edema - microbiology | Pneumonia, Bacterial - microbiology | Edema - immunology | Rats | Bacterial Proteins - physiology | Pseudomonas Infections - microbiology | Pseudomonas Infections - immunology | Endothelial Cells - immunology | Host-Pathogen Interactions | Animals | Lung Injury - microbiology | Pseudomonas Infections - pathology | Pneumonia, Bacterial - immunology | Lung - blood supply |