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The Journal of hospital infection, ISSN 0195-6701, 1980
Journal
Journal
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2008, Volume 321, Issue 5889, pp. 691 - 696
...). MyD88 deficiency in mice leads to susceptibility to a broad range of pathogens in experimental settings of infection... 
Receptors | Phenotypes | Transfection | Cytokines | HEK293 cells | Genes | Cell lines | Fibroblasts | Agonists | Reports | Children | MYD88-DEFICIENT MICE | HERPES-SIMPLEX-VIRUS | PROTECTIVE IMMUNITY | MYELOID DIFFERENTIATION FACTOR-88 | PSEUDOMONAS-AERUGINOSA | MULTIDISCIPLINARY SCIENCES | HUMORAL IMMUNITY | STAPHYLOCOCCUS-AUREUS | AERUGINOSA LUNG INFECTION | HOST RESPONSE | CUTTING EDGE | Humans | Child, Preschool | Male | Mutation, Missense | Bacterial Infections - genetics | Pneumococcal Infections - immunology | Bacterial Infections - immunology | Gene Deletion | Pneumococcal Infections - genetics | Female | Toll-Like Receptors - metabolism | Child | Staphylococcal Infections - genetics | Disease Susceptibility | Cytokines - metabolism | Signal Transduction | Staphylococcal Infections - immunology | Receptors, Interleukin-1 - immunology | Toll-Like Receptors - immunology | Myeloid Differentiation Factor 88 - genetics | Immunity, Innate | Pseudomonas Infections - genetics | Pseudomonas Infections - immunology | Receptors, Interleukin-1 - metabolism | Animals | Myeloid Differentiation Factor 88 - deficiency | Adolescent | Mice | Myeloid Differentiation Factor 88 - metabolism | Cell Line, Transformed | Genetic aspects | Bacterial infections | Pediatrics | Bacteria | Biomedical research | Genetic disorders | Immunology | Pneumococcal Infections | Life Sciences | Toll-Like Receptors | Bacterial Infections | Myeloid Differentiation Factor 88 | Bacteriology | Staphylococcal Infections | Microbiology and Parasitology | Pseudomonas Infections | Receptors, Interleukin-1
Journal Article
PLoS pathogens, ISSN 1553-7374, 2009, Volume 5, Issue 12, p. e1000703
We sought to define protective mechanisms of immunity to Staphylococcus aureus and Candida albicans bloodstream infections in mice immunized with the recombinant N-terminus of Als3p (rAls3p-N... 
RECOMBINANT N-TERMINUS | RISK-FACTORS | NEUTROPHIL | MACROPHAGES | MICROBIOLOGY | IMPROVES SURVIVAL | VIRULENCE | DAMAGE | VIROLOGY | INTERFERON-GAMMA | IL-17 | HOST-DEFENSE | PARASITOLOGY | Adaptive Immunity | T-Lymphocyte Subsets - immunology | Interferon-gamma | Adjuvants, Immunologic - pharmacology | Staphylococcal Infections - immunology | Mice, Inbred C57BL | Interleukin-17 - immunology | Vaccines - immunology | Fungal Vaccines - immunology | Adoptive Transfer | Candida albicans - immunology | Th1 Cells - immunology | Candidiasis - prevention & control | Animals | Fungal Proteins - immunology | Aluminum Hydroxide - immunology | Female | Staphylococcal Infections - prevention & control | Staphylococcus aureus - immunology | Mice | Mice, Inbred BALB C | Candidiasis - immunology | Candidiasis | Immune response | Staphylococcus aureus infections | Physiological aspects | Development and progression | Genetic aspects | Research | T cells | Pathogens | g-Interferon | Helper cells | Adjuvants | Data processing | Inflammation | Leukocytes (neutrophilic) | Lymphocytes T | Vaccines | Immunity | Interleukin 17 | virulence factors | CD4 antigen | Infection | Phagocytes | Aluminum hydroxide | N-Terminus | Public health | Immune system | Microorganisms | Microbiology | Cytokines | Lymphocytes | Staphylococcus infections | Organisms
Journal Article
Immunity (Cambridge, Mass.), ISSN 1074-7613, 2014, Volume 40, Issue 6, pp. 896 - 909
Animal host defense against infection requires the expression of defense genes at the right place and the right time... 
LIFE-SPAN | CAENORHABDITIS-ELEGANS | RECOGNITION | AUTOPHAGY GENES | REGULATES AUTOPHAGY | STAPHYLOCOCCUS-AUREUS | INFECTION | IMMUNOLOGY | PROTEINS | C. ELEGANS | LYSOSOMAL BIOGENESIS | Pseudomonas aeruginosa - immunology | Caenorhabditis elegans - microbiology | Transcriptional Activation - genetics | Caenorhabditis elegans Proteins - immunology | Salmonella Infections - immunology | Transcriptional Activation - immunology | Autophagy - immunology | Signal Transduction - immunology | RNA Interference | Autophagy - genetics | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - immunology | Macrophages - immunology | Enterococcus faecalis - immunology | Basic Helix-Loop-Helix Transcription Factors - genetics | Staphylococcal Infections - immunology | Immunity, Innate | Caenorhabditis elegans - immunology | Pseudomonas Infections - immunology | Animals | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - genetics | Salmonella enterica - immunology | Basic Helix-Loop-Helix Transcription Factors - immunology | Staphylococcus aureus - immunology | Mice | RNA, Small Interfering | Caenorhabditis elegans Proteins - genetics | Genetic aspects | Genetic transcription | Analysis | Gastrointestinal diseases | Genes | Genomics | Signal transduction | Transcription factors | Nematodes | Staphylococcus infections | Kinases | Mammals | Gene expression | Experiments | Autophagy | Chemokines
Journal Article
PloS one, ISSN 1932-6203, 2012, Volume 7, Issue 9, p. e41879
Secondary bacterial pneumonias are a frequent complication of influenza and other respiratory viral infections, but the mechanisms underlying viral-induced susceptibility to bacterial infections are poorly understood... 
TOLL-LIKE RECEPTOR-3 | COMMUNITY-ACQUIRED PNEUMONIA | DOUBLE-STRANDED-RNA | PANDEMIC INFLUENZA | MULTIDISCIPLINARY SCIENCES | CHRONIC HEPATITIS-C | RIG-I | MICROBIAL ETIOLOGY | NF-KAPPA-B | RESPIRATORY-TRACT INFECTION | INFLUENZA INFECTION | Poly I-C - administration & dosage | Antigens, Viral - administration & dosage | Interferon Type I - immunology | Streptococcus pneumoniae - immunology | Pneumococcal Infections - immunology | Pneumococcal Infections - genetics | Pneumonia, Bacterial - mortality | Pneumococcal Infections - microbiology | Pneumonia, Bacterial - genetics | Poly I-C - immunology | Receptor, Interferon alpha-beta - genetics | Staphylococcal Infections - microbiology | Toll-Like Receptor 3 - genetics | Aminoquinolines - pharmacology | Pneumonia, Bacterial - microbiology | Staphylococcal Infections - genetics | Disease Susceptibility | Nerve Tissue Proteins - immunology | Staphylococcal Infections - immunology | Membrane Proteins - genetics | Pneumococcal Infections - mortality | Membrane Proteins - immunology | Survival Rate | Toll-Like Receptor 3 - immunology | Imidazoles - pharmacology | Methicillin-Resistant Staphylococcus aureus - immunology | Nerve Tissue Proteins - genetics | Antibodies - pharmacology | Gene Expression Regulation - drug effects | Antigens, Viral - immunology | Staphylococcal Infections - mortality | Animals | Receptor, Interferon alpha-beta - immunology | Signal Transduction - drug effects | Interferon Type I - genetics | Pneumonia, Bacterial - immunology | Mice | Interferon Inducers - pharmacology | Pneumonia | Bacterial pneumonia | Influenza | Staphylococcus aureus infections | Bacteria | Disease susceptibility | Interferon | Nucleic acids | Health aspects | Antibacterial agents | Pandemics | Imiquimod | Immune clearance | Impairment | Gram-positive bacteria | Viruses | Infections | Drug resistance | Methicillin | Proteins | Toll-like receptors | Trachea | Immune system | Pathogens | Bacterial infections | Double-stranded RNA | Poly (I:C) | Signaling | Lungs | Ligands | Retinoic acid | Viral infections | Indexing in process
Journal Article
The Journal of experimental medicine, ISSN 1540-9538, 2014, Volume 211, Issue 12, pp. 2331 - 2339
Journal Article
Nature immunology, ISSN 1529-2916, 2016, Volume 17, Issue 6, pp. 626 - 635
... to being ILC1 cells that produced interferon-gamma (IFN-gamma). Interleukin 12 (IL-12) and IL-18 regulated this conversion, and during viral infection, ILC2 cells clustered within inflamed areas and acquired an ILC1-like phenotype... 
BET | PATHOGENESIS | NATURAL-KILLER-CELLS | CYTOKINES | PROGENITOR | ROR-GAMMA-T | TRANSCRIPTION FACTOR GATA3 | INFECTION | DIFFERENTIATION | IMMUNOLOGY | TYPE-1 | GATA3 Transcription Factor - genetics | Smoking - adverse effects | Humans | Middle Aged | Male | Th2 Cells - immunology | Cell Plasticity - immunology | Th1 Cells - immunology | Lymphocytes - immunology | Inflammation Mediators - metabolism | Female | Influenza A virus - immunology | Cell Differentiation | GATA3 Transcription Factor - metabolism | Cytokines - metabolism | Staphylococcal Infections - immunology | Mice, Inbred C57BL | Cells, Cultured | Gene Expression Regulation | Immunity, Innate | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Mice, Knockout | Phenotype | Animals | Haemophilus influenzae - immunology | Staphylococcus aureus - immunology | Aged | Mice | Haemophilus Infections - immunology | Pulmonary Disease, Chronic Obstructive - immunology | Lung - immunology | Orthomyxoviridae Infections - immunology | Physiological aspects | Phenotypic plasticity | Development and progression | Lung diseases, Obstructive | Lymphoid tissue | Health aspects | Basic Medicine | Immunologi inom det medicinska området | Medical and Health Sciences | Medicin och hälsovetenskap | Immunology in the medical area | Medicinska och farmaceutiska grundvetenskaper
Journal Article
PloS one, ISSN 1932-6203, 07/2014, Volume 9, Issue 7, p. e102606
The human hCLCA1 and its murine ortholog mCLCA3 (calcium-activated chloride channel regulators) are exclusively expressed in mucus cells and linked to... 
ACTIVATED CHLORIDE CHANNEL | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | DISEASE | AIRWAY EPITHELIUM | MUCUS OVERPRODUCTION | ACUTE LUNG INJURY | ASTHMA | CYSTIC-FIBROSIS | MODEL | EXPRESSION | Lung - microbiology | Mucoproteins - immunology | Interleukin-17 - immunology | Bronchoalveolar Lavage Fluid - immunology | Capillary Permeability - immunology | Chloride Channels - genetics | Pneumonia, Staphylococcal - microbiology | Cell Movement - immunology | Leukocytes - immunology | RNA, Messenger - biosynthesis | Female | Bronchoalveolar Lavage Fluid - cytology | Staphylococcal Infections - microbiology | Cytokines - immunology | Disease Models, Animal | Mucoproteins - genetics | Neutrophil Infiltration - immunology | Pneumonia, Staphylococcal - immunology | Lung - pathology | Staphylococcal Infections - immunology | Mice, Inbred C57BL | Cytokines - secretion | Neutrophils - immunology | Chemokine CXCL1 - biosynthesis | Inflammation | Interleukin-17 - biosynthesis | Random Allocation | Chloride Channels - immunology | Mice, Knockout | Mucins - biosynthesis | Chemokine CXCL1 - immunology | Immunity, Innate - immunology | Animals | Staphylococcus aureus - immunology | Mice | Staphylococcus aureus - growth & development | Lung - immunology | Pneumonia | Bacterial infections | RNA | Cytokines | Bacterial pneumonia | Mucins | Staphylococcus aureus infections | Permeability | Comparative analysis | Staphylococcus aureus | Asthma | Regulators | Immune clearance | Mucus | Immunity | Proteins | Histopathology | Respiratory tract diseases | Chronic obstructive pulmonary disease | Nosocomial infections | Pathogens | Pulmonary arteries | Bronchus | Leukocytes (neutrophilic) | Gene expression | Chloride channels (calcium-gated) | Interleukin 17 | Pathology | Metaplasia | Infectious diseases | Fibrosis | Immigration | Infiltration | Cell migration | Calcium | Inflammatory response | Homology | Innate immunity | Infections | Kinases | Macrophages | Rodents | Bacteria | Alveoli | Immune response | Lung diseases | Staphylococcus infections | Cystic fibrosis | Calcium chloride | White blood cells | Signaling | Lungs | Cell number | Laboratory animals | Viral infections
Journal Article
Infection and Immunity, ISSN 0019-9567, 03/2014, Volume 82, Issue 3, pp. 1192 - 1204
Classifications Services IAI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit... 
CARBON CATABOLITE REPRESSION | INFECTIOUS DISEASES | ESSENTIAL GENES | CCPA-MEDIATED REPRESSION | VIRULENCE FACTORS | BACILLUS-SUBTILIS | IN-VIVO | CYSTEINE PROTEASE SPEB | PYOGENES | STAPHYLOCOCCUS-AUREUS | IMMUNOLOGY | EXPRESSION | Soft Tissue Infections - immunology | Virulence Factors - genetics | Genes, Bacterial - genetics | Streptococcal Infections - metabolism | Staphylococcal Skin Infections - metabolism | Virulence Factors - immunology | Phosphoenolpyruvate Sugar Phosphotransferase System - immunology | Mutation - immunology | Exotoxins - metabolism | Streptococcal Infections - genetics | Streptococcus pyogenes - genetics | Genes, Bacterial - immunology | Soft Tissue Infections - genetics | Virulence - genetics | Staphylococcal Skin Infections - immunology | Female | Bacterial Proteins - immunology | Phosphoenolpyruvate Sugar Phosphotransferase System - genetics | Streptococcal Infections - microbiology | Streptolysins - metabolism | Streptococcus pyogenes - immunology | Exotoxins - immunology | Bacterial Proteins - genetics | Streptococcus pyogenes - metabolism | Carbohydrates - immunology | Mutation - genetics | Soft Tissue Infections - metabolism | Animals | Soft Tissue Infections - microbiology | Streptolysins - genetics | Virulence - immunology | Exotoxins - genetics | Phosphoenolpyruvate Sugar Phosphotransferase System - metabolism | Bacterial Proteins - metabolism | Virulence Factors - metabolism | Mice | Streptococcal Infections - immunology | Streptolysins - immunology | Staphylococcal Skin Infections - microbiology | Staphylococcal Skin Infections - genetics | Molecular Pathogenesis
Journal Article
American journal of physiology. Lung cellular and molecular physiology, ISSN 1522-1504, 2015, Volume 309, Issue 2, pp. L158 - L167
Suppression of type 17 immunity by type I interferon (IFN) during influenza A infection has been shown to enhance susceptibility to secondary bacterial pneumonia... 
Influenza A | Coinfection | Type I interferon | Escherichia coli | Staphylococcus aureus | UNITED-STATES | PHYSIOLOGY | influenza A | ESCHERICHIA-COLI | INNATE IMMUNE-RESPONSE | STAPHYLOCOCCUS-AUREUS PNEUMONIA | PULMONARY HOST-DEFENSE | type I interferon | STREPTOCOCCUS-PNEUMONIAE | PSEUDOMONAS-AERUGINOSA INFECTION | RESPIRATORY SYSTEM | LIPOCALIN 2 | coinfection | KLEBSIELLA-PNEUMONIAE | T-CELLS | Male | Receptor, Interferon alpha-beta - physiology | Antimicrobial Cationic Peptides - metabolism | Escherichia coli Infections - virology | Escherichia coli - pathogenicity | Influenza A virus - pathogenicity | Pneumonia - immunology | Influenza A virus - immunology | Staphylococcal Infections - microbiology | Staphylococcal Infections - virology | Pneumonia, Bacterial - microbiology | Disease Susceptibility | Staphylococcal Infections - immunology | Coinfection - immunology | Mice, Inbred C57BL | Orthomyxoviridae Infections - microbiology | Escherichia coli - immunology | Escherichia coli Infections - microbiology | Pneumonia - microbiology | Pneumonia, Bacterial - virology | Coinfection - virology | Pneumonia - virology | Staphylococcus aureus - pathogenicity | Mice, Knockout | Coinfection - microbiology | Animals | Escherichia coli Infections - immunology | Pneumonia, Bacterial - immunology | Staphylococcus aureus - immunology | Mice | Orthomyxoviridae Infections - virology | Orthomyxoviridae Infections - immunology | Complications and side effects | Medical research | Pneumonia | Bacterial pneumonia | Influenza | Medicine, Experimental | Disease susceptibility | Research | Risk factors | Comorbidity | Analysis | Staphylococcus aureus infections | Interferon | Biological response modifiers | Health aspects
Journal Article
PLoS pathogens, ISSN 1553-7374, 2017, Volume 13, Issue 1, p. e1006092
Toll/interleukin-1 receptor (TIR) domains in Toll-like receptors are essential for initiating and propagating the eukaryotic innate immune signaling cascade.... 
Laboratory of Phytopathology | EPS | Laboratorium voor Phytopathologie | Laboratorium voor Fytopathologie | STRAINS | SYSTEM | CONTAINING PROTEINS | MICROBIOLOGY | CASSETTE CHROMOSOME MEC | VECTOR | FAMILY | EVOLUTION | VIROLOGY | GENOMES | BTPB | CLONES | PARASITOLOGY | Virulence Factors - genetics | Humans | Receptors, Interleukin-1 - genetics | Penicillin-Binding Proteins - genetics | Virulence Factors - immunology | Signal Transduction - immunology | Staphylococcal Skin Infections - drug therapy | HEK293 Cells | Bacterial Proteins - immunology | Fusidic Acid - pharmacology | Membrane Glycoproteins - immunology | Macrophages - immunology | Disease Models, Animal | Staphylococcus aureus - genetics | Cell Line | Receptors, Interleukin-1 - immunology | Mice, Inbred C57BL | Bacterial Proteins - genetics | Myeloid Differentiation Factor 88 - genetics | Neutrophils - immunology | Staphylococcus aureus - pathogenicity | Membrane Glycoproteins - genetics | Mice, Knockout | Animals | Myeloid Differentiation Factor 88 - deficiency | Toll-Like Receptors - genetics | Staphylococcus aureus - immunology | Mice | Staphylococcal Skin Infections - microbiology | Bacterial infections | Disease transmission | Gene mutations | Analysis | Genetic aspects | Research | Bacterial genetics | Epidemiology | Risk factors | Studies | Pathogens | Medical research | Enzymes | Cytokines | Laboratories | Genes | Antimicrobial agents | Staphylococcus infections | Genetic engineering | Experiments | Life Sciences | Microbiology and Parasitology | Immunology | Bacteriology | Virology
Journal Article