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1. Full Text Development and Function of Invariant Natural Killer T Cells Producing T(H)2- and T(H)17-Cytokines
by Watarai, H and Sekine-Kondo, E and Shigeura, T and Motomura, Y and Yasuda, T and Satoh, R and Yoshida, H and Kubo, M and Kawamoto, H and Koseki, H and Taniguchi, M
PLOS BIOLOGY, ISSN 1545-7885, 02/2012, Volume 10, Issue 2, p. e1001255
There is heterogeneity in invariant natural killer T (iNKT) cells based on the expression of CD4 and the IL-17 receptor B (IL-17RB), a receptor for IL-25 which... 
V(ALPHA)14 NKT CELLS | IMMUNE-RESPONSE | ACTIVATION | SYNCYTIAL VIRUS-INFECTION | ROR-GAMMA-T | BIOCHEMISTRY & MOLECULAR BIOLOGY | AIRWAY HYPERREACTIVITY | MOUSE | BIOLOGY | RECEPTOR | MICE | SUBSET | Liver - pathology | Th2 Cells - physiology | Bronchial Hyperreactivity - immunology | Gene Expression Profiling | Receptors, Interleukin-17 - genetics | T-Lymphocyte Subsets - physiology | Respiratory Syncytial Virus Infections - immunology | Natural Killer T-Cells - physiology | Lung - virology | Flow Cytometry | Natural Killer T-Cells - pathology | Thymus Gland - pathology | Bronchial Hyperreactivity - metabolism | Receptors, Interleukin-17 - metabolism | Spleen - pathology | Th2 Cells - pathology | Th17 Cells - pathology | Lung - pathology | Th17 Cells - physiology | Cytokines - metabolism | Tissue Culture Techniques | Mice, Inbred C57BL | Cells, Cultured | Immunophenotyping | Organ Specificity | Mice, Knockout | Bronchial Hyperreactivity - virology | Bronchial Hyperreactivity - pathology | Animals | T-Lymphocyte Subsets - metabolism | Mice | Mice, Inbred BALB C | Respiratory Syncytial Virus Infections - pathology | Lung - immunology
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2. Full Text Interleukin-1β mediates virus-induced M2 muscarinic receptor dysfunction and airway hyperreactivity
by Rynko, Abby E and Fryer, Allison D and Jacoby, David B
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 10/2014, Volume 51, Issue 4, pp. 494 - 501
Respiratory viral infections are associated with the majority of asthma attacks. Inhibitory M2 receptors on parasympathetic nerves, which normally limit... 
Parainfluenza virus | TNF-α | IL-1β | Parasympathetic nerves | Asthma | Tumor Necrosis Factor-alpha - metabolism | Lung - innervation | Paramyxoviridae - pathogenicity | Bronchial Hyperreactivity - immunology | Bronchial Provocation Tests | Parasympathetic Nervous System - virology | Paramyxoviridae Infections - physiopathology | Lung - virology | Paramyxoviridae Infections - virology | Bronchoconstriction - drug effects | Interleukin-1beta - metabolism | Bronchial Hyperreactivity - physiopathology | Bronchial Hyperreactivity - metabolism | Lung - metabolism | Parasympathetic Nervous System - physiopathology | Interleukin 1 Receptor Antagonist Protein - pharmacology | Parasympathetic Nervous System - metabolism | Respiratory Tract Infections - virology | Respiratory Tract Infections - physiopathology | Disease Models, Animal | Respiratory Tract Infections - metabolism | Guinea Pigs | Paramyxoviridae Infections - metabolism | Receptor, Muscarinic M2 - metabolism | Signal Transduction | Lung - physiopathology | Bronchial Hyperreactivity - prevention & control | Bronchial Hyperreactivity - virology | Host-Pathogen Interactions | Paramyxoviridae Infections - immunology | Parasympathetic Nervous System - immunology | Paramyxoviridae - immunology | Animals | Lung - drug effects | Respiratory Tract Infections - immunology | Cell Line, Tumor | Lung - immunology | asthma | parasympathetic nerves | parainfluenza virus | Original Research
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3. Full Text MDA5 and TLR3 initiate pro-inflammatory signaling pathways leading to rhinovirus-induced airways inflammation and hyperresponsiveness
by Wang, Qiong and Miller, David J and Bowman, Emily R and Nagarkar, Deepti R and Schneider, Dina and Zhao, Ying and Linn, Marisa J and Goldsmith, Adam M and Bentley, J. Kelley and Sajjan, Umadevi S and Hershenson, Marc B
PLoS Pathogens, ISSN 1553-7366, 05/2011, Volume 7, Issue 5, p. e1002070
Rhinovirus (RV), a single-stranded RNA picornavirus, is the most frequent cause of asthma exacerbations. We previously demonstrated in human bronchial... 
DOUBLE-STRANDED-RNA | RECOGNITION | RIG-I | MICROBIOLOGY | EOSINOPHIL CATIONIC PROTEIN | TOLL-LIKE RECEPTOR-3 | ANTIVIRAL RESPONSES | VIROLOGY | EPITHELIAL-CELLS | DISEASE | RESPIRATORY-SYNCYTIAL-VIRUS | INFECTION | PARASITOLOGY | Lung Diseases - metabolism | Male | Rhinovirus - isolation & purification | Rhinovirus - physiology | Picornaviridae Infections - virology | Interferon-Induced Helicase, IFIH1 | DEAD-box RNA Helicases - physiology | Inflammation - metabolism | Lung - virology | Lung Diseases - virology | Bronchial Hyperreactivity - physiopathology | Bronchial Hyperreactivity - metabolism | Lung - metabolism | RNA, Double-Stranded - metabolism | RNA, Viral - metabolism | Picornaviridae Infections - metabolism | Disease Models, Animal | Mice, Inbred C57BL | Inflammation - virology | Lung - physiopathology | Mice, Knockout | Bronchial Hyperreactivity - virology | Toll-Like Receptor 3 - physiology | Animals | Interferons - metabolism | Picornaviridae Infections - physiopathology | Signal Transduction - physiology | Lung Diseases - physiopathology | Mice | Inflammation - physiopathology | Polymerase chain reaction | Usage | Rhinoviruses | Toll-like receptors | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Proteins | Viruses | Infections | Lymphocytes | Viral infections | Immune system
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4. Full Text Mouse models of rhinovirus-induced disease and exacerbation of allergic airway inflammation
by Bartlett, Nathan W and Killington, Richard A and Pedrick, Michael S and Edwards, Michael R and Blair, Edward D and Guy, Bruno and Rowlands, David J and Zhu, Jie and Papi, Alberto and Sharp, Nigel A and Almond, Jeffrey W and Choy, Katherine J and Johnston, Sebastian L and Schwarze, Jurgen and Hurle, Michael J and Tuthill, Tobias J and Jourdan, Patrick and Walton, Ross P and Glanville, Nicholas and Caramori, Gaetano and Bussell, James N and Clarke, Neil J and Aniscenko, Juliya and Burnet, Jerome and Swallow, Dallas M and Jeffery, Peter K and Lloyd, Clare M and Plumpton, Chris
Nature Medicine, ISSN 1078-8956, 02/2008, Volume 14, Issue 2, pp. 199 - 204
Rhinoviruses cause serious morbidity and mortality as the major etiological agents of asthma exacerbations and the common cold. A major obstacle to... 
MEDICINE, RESEARCH & EXPERIMENTAL | BRONCHIAL EPITHELIAL-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ICAM-1 | EFFICIENT REPLICATION | CHILDREN | CELL BIOLOGY | POTENT ANTIVIRAL ACTIVITY | IN-VIVO | INFECTION | EXPRESSION | SEVERITY | VIRUS-INDUCED ASTHMA | Respiratory System - pathology | Bronchial Hyperreactivity - immunology | Dendritic Cells - immunology | Humans | Th2 Cells - radiation effects | Hypersensitivity - immunology | Th2 Cells - immunology | Rhinovirus - physiology | Th1 Cells - immunology | Picornaviridae Infections - virology | Dendritic Cells - radiation effects | Respiratory System - virology | Virus Inactivation - radiation effects | Chemotactic Factors - biosynthesis | Respiratory System - radiation effects | Rhinovirus - radiation effects | Ultraviolet Rays | Neutrophils - radiation effects | Th1 Cells - radiation effects | Mucus - metabolism | Respiratory System - immunology | Chemokines - immunology | Disease Models, Animal | Inflammation Mediators - immunology | Chemokines - biosynthesis | Antibody Formation - radiation effects | Intercellular Adhesion Molecule-1 - immunology | Neutrophils - immunology | Mice, Transgenic | Inflammation | Hypersensitivity - virology | Bronchial Hyperreactivity - virology | Animals | Immunity, Innate - radiation effects | Virus Replication - radiation effects | Mice | Usage | Care and treatment | Rhinoviruses | Models | Research | Health aspects | Risk factors | Asthma | Pathology | Medical research | Cellular biology | Rodents | Viruses | Colds | Allergies
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5. Full Text CCL7 and IRF-7 mediate hallmark inflammatory and IFN responses following rhinovirus 1B infection
by Girkin, Jason and Hatchwell, Luke and Foster, Paul and Johnston, Sebastian L and Bartlett, Nathan and Collison, Adam and Mattes, Joerg
Journal of Immunology, ISSN 0022-1767, 05/2015, Volume 194, Issue 10, pp. 4924 - 4930
Rhinovirus (RV) infections are common and have the potential to exacerbate asthma. We have determined the lung transcriptome in RV strain 1B-infected naive... 
HYPERREACTIVITY | IMMUNE-RESPONSES | ALLERGIC AIRWAYS DISEASE | T(H)2 CELLS | ASTHMA | PROTEIN PHOSPHATASE 2A | IMMUNOLOGY | PATTERN-RECOGNITION RECEPTORS | EXACERBATION | EOTAXIN | CHILDREN | Bronchial Hyperreactivity - immunology | Inflammation - virology | NF-kappa B - immunology | Transcriptome | Male | Inflammation - immunology | Interferon Regulatory Factor-7 - immunology | Interferons - immunology | Common Cold - immunology | Bronchial Hyperreactivity - virology | Animals | Flow Cytometry | Chemokine CCL7 - immunology | Mice | Mice, Inbred BALB C | Rhinovirus - immunology | Real-Time Polymerase Chain Reaction | Lung - immunology | Disease Models, Animal
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6. Full Text Toll-like receptor-2/6 and toll-like receptor-9 agonists suppress viral replication but not airway hyperreactivity in guinea pigs
by Drake, Matthew G and Evans, Scott E and Dickey, Burton F and Fryer, Allison D and Jacoby, David B
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 06/2013, Volume 48, Issue 6, pp. 790 - 796
Respiratory virus infections cause airway hyperreactivity (AHR). Preventative strategies for virus-induced AHR remain limited. Toll-like receptors (TLRs) have... 
Airway hyperreactivity | Parainfluenza virus | Muscarinic receptor | Toll-like receptor | PULMONARY PARASYMPATHETIC NERVES | airway hyperreactivity | DIFFERENTIAL EXPRESSION | VIRUS-INFECTION | DENDRITIC CELLS | MUSCARINIC RECEPTORS | BIOCHEMISTRY & MOLECULAR BIOLOGY | muscarinic receptor | CELL BIOLOGY | SMOOTH-MUSCLE | RESPIRATORY SYSTEM | INFLAMMATION | TLR9 | ASTHMA | parainfluenza virus | INNATE IMMUNITY | Toll-Like Receptor 2 - agonists | Bronchial Hyperreactivity - immunology | Lipopeptides - pharmacology | Receptor, Muscarinic M3 - drug effects | Respirovirus Infections - drug therapy | Respirovirus Infections - virology | Toll-Like Receptor 9 - agonists | Toll-Like Receptor 9 - immunology | Receptor, Muscarinic M3 - immunology | Bronchoconstriction | Lung - virology | Toll-Like Receptor 6 - immunology | Bronchial Hyperreactivity - physiopathology | Female | Leukocyte Count | Respirovirus Infections - immunology | Sendai virus - physiology | Virus Replication - drug effects | Antiviral Agents - pharmacology | Guinea Pigs | Specific Pathogen-Free Organisms | Acetylcholine - pharmacology | Sendai virus - immunology | Respirovirus Infections - physiopathology | Bronchial Hyperreactivity - virology | Drug Synergism | Animals | Lung - drug effects | Toll-Like Receptor 2 - immunology | Oligodeoxyribonucleotides - pharmacology | Lung - immunology | Toll-Like Receptor 6 - agonists
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7. Full Text Neonatal bronchial hyperresponsiveness precedes acute severe viral bronchiolitis in infants
by Chawes, Bo L.K., MD, PhD and Poorisrisak, Porntiva, MD, PhD and Johnston, Sebastian L., MD, PhD and Bisgaard, Hans, MD, DMSc
Journal of Allergy and Clinical Immunology, The, ISSN 0091-6749, 2012, Volume 130, Issue 2, pp. 354 - 361.e3
Background Respiratory syncytial virus and other respiratory tract viruses lead to common colds in most infants, whereas a minority develop acute severe... 
Allergy and Immunology | lung function measurements | viral bronchiolitis | infants | Bronchial responsiveness | HIGH-RISK CHILDREN | EARLY-LIFE | PREDISPOSING FACTOR | LUNG-FUNCTION | IMMUNOLOGY | PROSPECTIVE BIRTH COHORT | YOUNG INFANTS | CHILDHOOD ASTHMA | ATOPIC-DERMATITIS | ALLERGY | RHINOVIRUS ILLNESSES | RESPIRATORY-SYNCYTIAL-VIRUS | Severity of Illness Index | Acute Disease | Prospective Studies | Bronchial Hyperreactivity - immunology | Humans | Respiratory Syncytial Viruses - immunology | Bronchial Provocation Tests | Methacholine Chloride - immunology | Child, Preschool | Infant | Male | Bronchiolitis, Viral - virology | Bronchial Hyperreactivity - complications | Respiratory Syncytial Virus Infections - immunology | Bronchial Hyperreactivity - virology | Time Factors | Female | Respiratory Function Tests | Respiratory Syncytial Virus Infections - virology | Bronchiolitis, Viral - complications | Infant, Newborn | Respiratory Syncytial Virus Infections - complications | Bronchiolitis, Viral - immunology | Virus diseases | Infants (Newborn) | Asthma in children | Respiratory tract diseases | Infants | Universities and colleges | Health aspects | Bronchiolitis | Babies | Studies | Viruses | Respiratory diseases | Age | Asthma | Neonates | Compression | Oxygen | Bronchopneumonia | Lung | Common cold | Pressure | Infection | Respiratory tract | Algorithms | Children | methacholine
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8. Full Text CXCR2 Is Required for Neutrophilic Airway Inflammation and Hyperresponsiveness in a Mouse Model of Human Rhinovirus Infection
by Nagarkar, Deepti R and Wang, Qiong and Shim, Jee and Zhao, Ying and Tsai, Wan C and Lukacs, Nicholas W and Sajjan, Uma and Hershenson, Marc B
The Journal of Immunology, ISSN 0022-1767, 11/2009, Volume 183, Issue 10, pp. 6698 - 6707
Human rhinovirus (RV) infection is responsible for the majority of virus-induced asthma exacerbations. Using a mouse model of human RV infection, we sought to... 
VIRUS | EPITHELIAL-CELLS | COMMON COLD | BONE-MARROW | RECEPTOR | SMOOTH-MUSCLE-CELLS | SUBJECTS IN-VIVO | ASTHMATIC SUBJECTS | IMMUNOLOGY | EXPRESSION | NONASTHMATIC SUBJECTS | Tumor Necrosis Factor-alpha - metabolism | Bronchial Hyperreactivity - immunology | Receptors, Tumor Necrosis Factor, Type I - immunology | Humans | Receptors, Tumor Necrosis Factor, Type I - metabolism | Picornaviridae Infections - virology | Lung - virology | Tumor Necrosis Factor-alpha - immunology | Bronchial Hyperreactivity - metabolism | Lung - metabolism | Chemokine CXCL1 - metabolism | Chemokine CXCL2 - metabolism | Neutrophils - metabolism | Picornaviridae Infections - metabolism | Disease Models, Animal | Rhinovirus | Lung - pathology | Picornaviridae Infections - immunology | Asthma - physiopathology | Mucin-5B - immunology | Mice, Inbred C57BL | Neutrophils - immunology | RNA, Viral - analysis | Receptors, Interleukin-8B - immunology | Receptors, Tumor Necrosis Factor, Type I - genetics | Neutrophils - virology | Mice, Knockout | Bronchial Hyperreactivity - virology | Chemokine CXCL1 - immunology | Mucin-5B - metabolism | Chemokine CXCL2 - immunology | Animals | Receptors, Interleukin-8B - metabolism | Receptors, Interleukin-8B - genetics | Mice | Mice, Inbred BALB C | Lung - immunology
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9. Full Text Human Rhinovirus 1B Exposure Induces Phosphatidylinositol 3-Kinase-dependent Airway Inflammation in Mice
by Newcomb, Dawn C and Sajjan, Umadevi S and Nagarkar, Deepti R and Wang, Qiong and Nanua, Suparna and Zhou, Ying and McHenry, Christina L and Hennrick, Kenneth T and Tsai, Wan C and Bentley, J. Kelley and Lukacs, Nicholas W and Johnston, Sebastian L and Hershenson, Marc B
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 05/2008, Volume 177, Issue 10, pp. 1111 - 1121
Rationale: Infection with rhinovirus (RV) triggers exacerbations of asthma and chronic obstructive lung disease. Objectives: We sought to develop a mouse model... 
Chronic obstructive pulmonary disease | Akt | Low-density lipoprotein receptor | Asthma | RESPIRATORY VIRUSES | INTERCELLULAR-ADHESION MOLECULE-1 | low-density lipoprotein receptor | RECEPTOR | asthma | EFFICIENT REPLICATION | NEUTROPHIL RECRUITMENT | ACUTE EXACERBATIONS | INDUCED SPUTUM | RESPIRATORY SYSTEM | GENE-EXPRESSION | INFECTION | chronic obstructive pulmonary disease | CRITICAL CARE MEDICINE | Bronchial Hyperreactivity - immunology | Humans | Pulmonary Disease, Chronic Obstructive - virology | Rhinovirus - pathogenicity | Phosphatidylinositol 3-Kinases - metabolism | Pneumonia - immunology | Female | Asthma - virology | Oncogene Protein v-akt - metabolism | Disease Models, Animal | Picornaviridae Infections - immunology | Signal Transduction | Neutrophils - immunology | Pulmonary Disease, Chronic Obstructive - complications | Chemotaxis | Pneumonia - virology | Bronchial Hyperreactivity - virology | Animals | Asthma - complications | Epithelial Cells - immunology | Epithelial Cells - virology | Picornaviridae Infections - physiopathology | Oncogene Protein v-akt - immunology | Chemokines - metabolism | Mice | D. Pulmonary Infections
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10. Full Text MMP-12-mediated by SARM-TRIF signaling pathway contributes to IFN-γ-independent airway inflammation and AHR post RSV infection in nude mice
by Long, Xiaoru and Li, Simin and Xie, Jun and Li, Wei and Zang, Na and Ren, Luo and Deng, Yu and Xie, Xiaohong and Wang, Lijia and Fu, Zhou and Liu, Enmei
Respiratory Research, ISSN 1465-9921, 02/2015, Volume 16, Issue 1, pp. 11 - 11
Background: Respiratory syncytial virus (RSV) is one of the most frequently observed pathogens during infancy and childhood. However, the corresponding... 
MMP-12 | AHR | Airway inflammation | RSV | TRIF | SARM | NATURAL-KILLER-CELLS | ACTIVATION | MATRIX METALLOPROTEINASE-12 | PROTEIN | METALLOPROTEINASE PRODUCTION | MACROPHAGES | FIBROBLASTS | RESPONSES | OBSTRUCTIVE PULMONARY-DISEASE | RESPIRATORY SYSTEM | RESPIRATORY SYNCYTIAL VIRUS | Pneumonia - physiopathology | Bronchial Hyperreactivity - immunology | T-Lymphocytes - enzymology | Cytoskeletal Proteins - genetics | Bronchoalveolar Lavage Fluid - immunology | Armadillo Domain Proteins - genetics | Interferon-gamma - metabolism | Adaptor Proteins, Vesicular Transport - metabolism | T-Lymphocytes - virology | Lung - enzymology | RNA Interference | Time Factors | Pneumonia - immunology | Respiratory Syncytial Virus, Human - pathogenicity | Respiratory Syncytial Virus Infections - enzymology | Disease Models, Animal | Pneumonia - genetics | Signal Transduction | Pneumonia - enzymology | Matrix Metalloproteinase 12 - immunology | Lung - physiopathology | Adaptor Proteins, Vesicular Transport - immunology | Matrix Metalloproteinase 12 - metabolism | Host-Pathogen Interactions | Matrix Metalloproteinase Inhibitors - pharmacology | Mice, Nude | Respiratory Syncytial Virus, Human - immunology | Lung - drug effects | T-Lymphocytes - immunology | Mice, Inbred BALB C | Immunity, Cellular | Respiratory Syncytial Virus Infections - immunology | Bronchoconstriction | Lung - virology | Bronchial Hyperreactivity - physiopathology | Respiratory Syncytial Virus Infections - physiopathology | Cytoskeletal Proteins - metabolism | Female | Respiratory Syncytial Virus Infections - virology | Respiratory Syncytial Virus Infections - genetics | Armadillo Domain Proteins - immunology | Pneumonia - virology | Bronchial Hyperreactivity - virology | Bronchial Hyperreactivity - enzymology | Animals | Cytoskeletal Proteins - immunology | Interferon-gamma - immunology | Armadillo Domain Proteins - metabolism | Lung - immunology | Research
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11. Full Text Differential Immune Responses and Pulmonary Pathophysiology Are Induced by Two Different Strains of Respiratory Syncytial Virus
by Lukacs, Nicholas W and Moore, Martin L and Rudd, Brian D and Berlin, Aaron A and Collins, Robert D and Olson, Sandra J and Ho, Samuel B and Peebles, R. Stokes
The American Journal of Pathology, ISSN 0002-9440, 2006, Volume 169, Issue 3, pp. 977 - 986
In this study we performed comparisons of pulmonary responses between two different respiratory syncytial virus (RSV) antigenic subgroup A strains, A2 and Line... 
IN-VITRO | PROTEIN | MYELOID DENDRITIC CELLS | GLYCOPROTEIN-G | LUNG-DISEASE | AIRWAY HYPERRESPONSIVENESS | INFECTION | MICE | PATHOLOGY | RSV CHALLENGE | T-CELLS | Dose-Response Relationship, Immunologic | Hyperplasia - immunology | Bronchial Hyperreactivity - immunology | Species Specificity | Respiratory Syncytial Viruses - immunology | Interleukin-13 - immunology | Mucins - immunology | Respiratory Syncytial Virus Infections - immunology | Goblet Cells - immunology | Bronchial Hyperreactivity - physiopathology | Respiratory Syncytial Virus Infections - physiopathology | Cell Line | Gene Expression Regulation - immunology | Mucin 5AC | Interleukin-13 - deficiency | Goblet Cells - virology | Hyperplasia - virology | Mice, Knockout | Bronchial Hyperreactivity - virology | Hyperplasia - pathology | Bronchial Hyperreactivity - pathology | Animals | Hyperplasia - physiopathology | Mice | Goblet Cells - pathology | Respiratory Syncytial Virus Infections - pathology | Regular
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12. Full Text Dual role of interleukin‐10 in the regulation of respiratory syncitial virus (RSV)‐induced lung inflammation
by Sun, L and Cornell, T. T and LeVine, A and Berlin, A. A and Hinkovska‐Galcheva, V and Fleszar, A. J and Lukacs, N. W and Shanley, T. P
Clinical & Experimental Immunology, ISSN 0009-9104, 05/2013, Volume 172, Issue 2, pp. 263 - 279
Summary RSV lower respiratory tract infections (LRTI) are among the most common diseases necessitating hospital admission in children. In addition to causing... 
pulmonary inflammation | Th2 cytokines | RSV | chemokines | Th1 | Pulmonary inflammation | Chemokines | IMMUNE-RESPONSE | DENDRITIC CELL | ALLERGIC AIRWAY INFLAMMATION | IMMUNOLOGY | VIRAL-INFECTION | IL-10 | IN-VIVO | DISEASE | ASTHMA | EXPRESSION | T-CELLS | Bronchial Hyperreactivity - immunology | Respiratory Syncytial Viruses - immunology | Interleukin-13 | Chemokine CCL2 - genetics | Mice, Transgenic | Th2 Cells - immunology | Pneumonia - virology | Respiratory Syncytial Virus Infections - immunology | Bronchial Hyperreactivity - virology | Lymphocyte Activation - immunology | Animals | Respiratory Tract Infections - immunology | Interleukin-10 - metabolism | Myeloid Cells - metabolism | Pneumonia - immunology | Chemokine CCL5 - metabolism | Mice | Respiratory Tract Infections - virology | Respiratory Syncytial Virus Infections - virology | Respiratory Syncytial Viruses - metabolism | Virus diseases | Bacterial infections | Interleukins | Analysis | Genetic engineering | Inflammation | Health aspects | Asthma | Infections | Cytokines | Rodents | Original
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13. Full Text Th17 cytokines are critical for respiratory syncytial virus-associated airway hyperreponsiveness through regulation by complement C3a and tachykinins
by Bera, Monali M and Lu, Bao and Martin, Thomas R and Cui, Shun and Rhein, Lawrence M and Gerard, Craig and Gerard, Norma P
Journal of Immunology, ISSN 0022-1767, 10/2011, Volume 187, Issue 8, pp. 4245 - 4255
Respiratory syncytial virus (RSV) infection is associated with serious lung disease in infants and immunocompromised individuals and is linked to development... 
ANAPHYLATOXIN RECEPTOR | ALLERGIC-ASTHMA | DISEASE | G-GLYCOPROTEIN | INFECTION | IMMUNOLOGY | EXPRESSION | PULMONARY EOSINOPHILIA | T-CELLS | SUBSTANCE-P RECEPTOR | CUTTING EDGE | Gene Expression | Bronchial Hyperreactivity - immunology | Cytokines - metabolism | Enzyme-Linked Immunosorbent Assay | Tachykinins - metabolism | Cell Separation | Respiratory Syncytial Viruses - immunology | Interleukin-17 - immunology | Gene Expression Profiling | Respiratory Syncytial Virus Infections - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Respiratory Syncytial Virus Infections - immunology | Mice, Knockout | Tachykinins - immunology | Bronchial Hyperreactivity - virology | Interleukin-17 - metabolism | Animals | Flow Cytometry | Bronchial Hyperreactivity - metabolism | Mice | Complement C3a - immunology | Complement C3a - metabolism | Cytokines - immunology
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14. Full Text Matrix metalloproteinase 9 exerts antiviral activity against respiratory syncytial virus
by Dabo, Abdoulaye J and Cummins, Neville and Eden, Edward and Geraghty, Patrick
PLoS ONE, ISSN 1932-6203, 08/2015, Volume 10, Issue 8, p. e0135970
Increased lung levels of matrix metalloproteinase 9 (MMP9) are frequently observed during respiratory syncytial virus (RSV) infection and elevated MMP9... 
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