世界胃肠病学杂志:英文版(电子版), ISSN 1007-9327, 2014, Volume 20, Issue 5, pp. 1165 - 1179
A complex mucosal barrier protects as the first line of defense the surface of the healthy intestinal tract from adhesion and invasion by luminal...
Antimicrobial | peptide | Mucus | barrier | lay | Intestinal | Inflammatory bowel disease | Paneth cell | Goblet cell | Intestinal barrier | Mucus layer | Crohn's disease | Antimicrobial peptide | Ulcerative colitis | EPITHELIAL TIGHT JUNCTIONS | INVASIVE ESCHERICHIA-COLI | ULCERATIVE-COLITIS | CELL ALPHA-DEFENSINS | ANTIMICROBIAL PEPTIDES | ILEAL CROHNS-DISEASE | 2 MUCUS LAYERS | HOST-DEFENSE | PANETH CELLS | GASTROENTEROLOGY & HEPATOLOGY | INNATE IMMUNITY | Intestinal Mucosa - metabolism | Colitis, Ulcerative - metabolism | Humans | Crohn Disease - metabolism | Colitis, Ulcerative - pathology | Intestinal Mucosa - microbiology | Permeability | Dysbiosis | Colitis, Ulcerative - immunology | Crohn Disease - immunology | Host-Pathogen Interactions | Animals | Colitis, Ulcerative - microbiology | Crohn Disease - pathology | Intestinal Mucosa - immunology | Crohn Disease - microbiology | Intestinal Mucosa - pathology | Topic Highlight | Crohn’s disease
Antimicrobial | peptide | Mucus | barrier | lay | Intestinal | Inflammatory bowel disease | Paneth cell | Goblet cell | Intestinal barrier | Mucus layer | Crohn's disease | Antimicrobial peptide | Ulcerative colitis | EPITHELIAL TIGHT JUNCTIONS | INVASIVE ESCHERICHIA-COLI | ULCERATIVE-COLITIS | CELL ALPHA-DEFENSINS | ANTIMICROBIAL PEPTIDES | ILEAL CROHNS-DISEASE | 2 MUCUS LAYERS | HOST-DEFENSE | PANETH CELLS | GASTROENTEROLOGY & HEPATOLOGY | INNATE IMMUNITY | Intestinal Mucosa - metabolism | Colitis, Ulcerative - metabolism | Humans | Crohn Disease - metabolism | Colitis, Ulcerative - pathology | Intestinal Mucosa - microbiology | Permeability | Dysbiosis | Colitis, Ulcerative - immunology | Crohn Disease - immunology | Host-Pathogen Interactions | Animals | Colitis, Ulcerative - microbiology | Crohn Disease - pathology | Intestinal Mucosa - immunology | Crohn Disease - microbiology | Intestinal Mucosa - pathology | Topic Highlight | Crohn’s disease
Journal Article
Infection and Immunity, ISSN 0019-9567, 10/2004, Volume 72, Issue 10, pp. 5750 - 5758
Classifications Services IAI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit...
INFECTIOUS DISEASES | INFLAMMATORY-BOWEL-DISEASE | CROHNS-DISEASE | HUMAN BETA-DEFENSIN-2 | LACTIC-ACID BACTERIA | ULCERATIVE-COLITIS | HOST-DEFENSE | ANTIMICROBIAL PEPTIDES | PANETH CELLS | IMMUNOLOGY | STRAIN NISSLE-1917 | INNATE IMMUNITY | Host Response and Inflammation
INFECTIOUS DISEASES | INFLAMMATORY-BOWEL-DISEASE | CROHNS-DISEASE | HUMAN BETA-DEFENSIN-2 | LACTIC-ACID BACTERIA | ULCERATIVE-COLITIS | HOST-DEFENSE | ANTIMICROBIAL PEPTIDES | PANETH CELLS | IMMUNOLOGY | STRAIN NISSLE-1917 | INNATE IMMUNITY | Host Response and Inflammation
Journal Article
Gut, ISSN 0017-5749, 12/2012, Volume 61, Issue 12, pp. 1693 - 1700
Objective The authors tested whether the anti-interleukin (IL)-17A monoclonal antibody secukinumab was safe and effective for the treatment of active Crohn's...
IMMUNITY | NECROSIS-FACTOR | INFLAMMATORY-BOWEL-DISEASE | COLITIS | SUSCEPTIBILITY LOCI | IL-23 | GASTROENTEROLOGY & HEPATOLOGY | CHRONIC MUCOCUTANEOUS CANDIDIASIS | CERTOLIZUMAB PEGOL | CLINICAL-RESPONSE | GENOME-WIDE ASSOCIATION | Biomarkers - metabolism | Severity of Illness Index | Crohn Disease - genetics | Double-Blind Method | Drug Administration Schedule | Humans | Leukocyte L1 Antigen Complex - metabolism | Middle Aged | Interleukin-17 - genetics | Antibodies, Monoclonal - therapeutic use | Male | Genetic Markers | Young Adult | Interleukin-17 - antagonists & inhibitors | Crohn Disease - drug therapy | Treatment Failure | Adolescent | Bayes Theorem | Anti-Inflammatory Agents - therapeutic use | Adult | Female | Aged | Polymorphism, Single Nucleotide | Infusions, Intravenous | Safety and security measures | Patient outcomes | Monoclonal antibodies | Dosage and administration | Crohn's disease | Research | Drug therapy | Hypothesis testing | Biomedical research | Psoriasis | Cytokines | Pathogenesis | Genomes | Inflammation | Patients | Crohns disease | Inflammatory bowel disease | Studies | Prescription drugs | Hypotheses | Gangrene | Pharmaceutical industry
IMMUNITY | NECROSIS-FACTOR | INFLAMMATORY-BOWEL-DISEASE | COLITIS | SUSCEPTIBILITY LOCI | IL-23 | GASTROENTEROLOGY & HEPATOLOGY | CHRONIC MUCOCUTANEOUS CANDIDIASIS | CERTOLIZUMAB PEGOL | CLINICAL-RESPONSE | GENOME-WIDE ASSOCIATION | Biomarkers - metabolism | Severity of Illness Index | Crohn Disease - genetics | Double-Blind Method | Drug Administration Schedule | Humans | Leukocyte L1 Antigen Complex - metabolism | Middle Aged | Interleukin-17 - genetics | Antibodies, Monoclonal - therapeutic use | Male | Genetic Markers | Young Adult | Interleukin-17 - antagonists & inhibitors | Crohn Disease - drug therapy | Treatment Failure | Adolescent | Bayes Theorem | Anti-Inflammatory Agents - therapeutic use | Adult | Female | Aged | Polymorphism, Single Nucleotide | Infusions, Intravenous | Safety and security measures | Patient outcomes | Monoclonal antibodies | Dosage and administration | Crohn's disease | Research | Drug therapy | Hypothesis testing | Biomedical research | Psoriasis | Cytokines | Pathogenesis | Genomes | Inflammation | Patients | Crohns disease | Inflammatory bowel disease | Studies | Prescription drugs | Hypotheses | Gangrene | Pharmaceutical industry
Journal Article
Journal of Molecular Medicine, ISSN 0946-2716, 1/2017, Volume 95, Issue 1, pp. 21 - 28
It is nowadays generally accepted that the microbiome is a central driver of chronic inflammatory bowel diseases based on observations from human patients as...
Human Genetics | Microbiota | Inflammatory bowel diseases | Biomedicine | Antimicrobial peptides | Internal Medicine | Molecular Medicine | Paneth cells | Endotoxin | LPS | MEDICINE, RESEARCH & EXPERIMENTAL | CROHNS-DISEASE | INTESTINAL MICROBIOTA | FECAL MICROBIOTA | ULCERATIVE-COLITIS | ALPHA-DEFENSINS | GUT MICROBIOTA | COLI NISSLE 1917 | RECURRENT CLOSTRIDIUM-DIFFICILE | HUMAN BETA-DEFENSIN-2 | GENETICS & HEREDITY | Paneth cells Inflammatory bowel diseases | CELL POLARIZATION | Intestinal Mucosa - metabolism | Signal Transduction | Humans | Gastrointestinal Microbiome | Adaptation, Biological | Lipopolysaccharides - metabolism | Intestinal Mucosa - microbiology | Antimicrobial Cationic Peptides - metabolism | Inflammatory Bowel Diseases - metabolism | Lipopolysaccharides - immunology | Antimicrobial Cationic Peptides - therapeutic use | Host-Pathogen Interactions - immunology | Animals | Intestinal Mucosa - immunology | Inflammatory Bowel Diseases - etiology | Inflammatory Bowel Diseases - therapy | Intestinal Mucosa - pathology | Genetic aspects | Microbiota (Symbiotic organisms) | Analysis | Animal models | Peptides | Mucosa | Microbiomes | Antiinfectives and antibacterials | Diseases | Microorganisms | Defensins | Intestine | Bowel disease | Rodents | Genetic factors
Human Genetics | Microbiota | Inflammatory bowel diseases | Biomedicine | Antimicrobial peptides | Internal Medicine | Molecular Medicine | Paneth cells | Endotoxin | LPS | MEDICINE, RESEARCH & EXPERIMENTAL | CROHNS-DISEASE | INTESTINAL MICROBIOTA | FECAL MICROBIOTA | ULCERATIVE-COLITIS | ALPHA-DEFENSINS | GUT MICROBIOTA | COLI NISSLE 1917 | RECURRENT CLOSTRIDIUM-DIFFICILE | HUMAN BETA-DEFENSIN-2 | GENETICS & HEREDITY | Paneth cells Inflammatory bowel diseases | CELL POLARIZATION | Intestinal Mucosa - metabolism | Signal Transduction | Humans | Gastrointestinal Microbiome | Adaptation, Biological | Lipopolysaccharides - metabolism | Intestinal Mucosa - microbiology | Antimicrobial Cationic Peptides - metabolism | Inflammatory Bowel Diseases - metabolism | Lipopolysaccharides - immunology | Antimicrobial Cationic Peptides - therapeutic use | Host-Pathogen Interactions - immunology | Animals | Intestinal Mucosa - immunology | Inflammatory Bowel Diseases - etiology | Inflammatory Bowel Diseases - therapy | Intestinal Mucosa - pathology | Genetic aspects | Microbiota (Symbiotic organisms) | Analysis | Animal models | Peptides | Mucosa | Microbiomes | Antiinfectives and antibacterials | Diseases | Microorganisms | Defensins | Intestine | Bowel disease | Rodents | Genetic factors
Journal Article
Deutsche Medizinische Wochenschrift, ISSN 0012-0472, 07/2018, Volume 113, Issue 13, pp. 953 - 959
Journal Article
DMW - Deutsche Medizinische Wochenschrift, ISSN 0012-0472, 07/2018, Volume 113, Issue 13, pp. 953 - 959
Abstract New promising treatment options for chronic inflammatory bowel diseases, confirm the expanded pathophysiological understanding in terms of the...
Dossier
Dossier
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 01/2006, Volume 281, Issue 4, pp. 2005 - 2011
Production of inducible antimicrobial peptides offers a first and rapid defense response of epithelial cells against invading microbes. Human beta-defensin-2...
HUMAN BETA-DEFENSINS | CROHNS-DISEASE | HUMAN BETA-DEFENSIN-2 | BIOCHEMISTRY & MOLECULAR BIOLOGY | INNATE IMMUNE-RESPONSE | TOLL-LIKE RECEPTORS | STAPHYLOCOCCUS-AUREUS | NF-KAPPA-B | INTESTINAL EPITHELIAL-CELLS | ANTIINFLAMMATORY SESQUITERPENE LACTONE | CAG PATHOGENICITY ISLAND | Epithelial Cells - metabolism | Frameshift Mutation | Luciferases - metabolism | Anti-Infective Agents - pharmacology | Humans | Peptidoglycan - chemistry | Crohn Disease - metabolism | NF-kappa B - metabolism | Transcription Factor AP-1 - metabolism | Transfection | Binding Sites | Genes, Reporter | RNA - metabolism | Cell Line | Promoter Regions, Genetic | Biotinylation | Mutagenesis, Site-Directed | Enzyme-Linked Immunosorbent Assay | Peptides - chemistry | Antimicrobial Cationic Peptides - chemistry | Down-Regulation | Antimicrobial Cationic Peptides - pharmacology | Nod2 Signaling Adaptor Protein | Reverse Transcriptase Polymerase Chain Reaction | Plasmids - metabolism | Keratinocytes - metabolism | beta-Defensins - pharmacology | Ligands | Mutation | Sesquiterpenes - pharmacology | Intracellular Signaling Peptides and Proteins - physiology | DNA, Complementary - metabolism | RNA, Small Interfering - metabolism
HUMAN BETA-DEFENSINS | CROHNS-DISEASE | HUMAN BETA-DEFENSIN-2 | BIOCHEMISTRY & MOLECULAR BIOLOGY | INNATE IMMUNE-RESPONSE | TOLL-LIKE RECEPTORS | STAPHYLOCOCCUS-AUREUS | NF-KAPPA-B | INTESTINAL EPITHELIAL-CELLS | ANTIINFLAMMATORY SESQUITERPENE LACTONE | CAG PATHOGENICITY ISLAND | Epithelial Cells - metabolism | Frameshift Mutation | Luciferases - metabolism | Anti-Infective Agents - pharmacology | Humans | Peptidoglycan - chemistry | Crohn Disease - metabolism | NF-kappa B - metabolism | Transcription Factor AP-1 - metabolism | Transfection | Binding Sites | Genes, Reporter | RNA - metabolism | Cell Line | Promoter Regions, Genetic | Biotinylation | Mutagenesis, Site-Directed | Enzyme-Linked Immunosorbent Assay | Peptides - chemistry | Antimicrobial Cationic Peptides - chemistry | Down-Regulation | Antimicrobial Cationic Peptides - pharmacology | Nod2 Signaling Adaptor Protein | Reverse Transcriptase Polymerase Chain Reaction | Plasmids - metabolism | Keratinocytes - metabolism | beta-Defensins - pharmacology | Ligands | Mutation | Sesquiterpenes - pharmacology | Intracellular Signaling Peptides and Proteins - physiology | DNA, Complementary - metabolism | RNA, Small Interfering - metabolism
Journal Article
Journal of Translational Medicine, ISSN 1479-5876, 12/2011, Volume 9, Issue S2, pp. I14 - I14
Secretory cells like the Paneth cell of the small intestinal crypt as well as mucin producing goblet cells seem to be of major importance in the initial...
Medical research | Small intestine | Bowel disease
Medical research | Small intestine | Bowel disease
Journal Article
F1000Research, ISSN 2046-1402, 2018, Volume 7, p. 1207
The so-called "biologicals" (monoclonal antibodies to various inflammatory targets like tumor necrosis factor or integrins) have revolutionized the treatment...
Therapy | Small molecules | Biologicals | Ulcerative colitis | Drugs | Inflammatory bowel diseases | Clinical trials | Histology | Inflammation | Gene expression | Patients | Marketing | Inflammatory bowel disease | Intestine | Monoclonal antibodies | Tumor necrosis factor-TNF | Remission | Colon | Endoscopy | Pharmaceutical industry | Azathioprine | Integrins
Therapy | Small molecules | Biologicals | Ulcerative colitis | Drugs | Inflammatory bowel diseases | Clinical trials | Histology | Inflammation | Gene expression | Patients | Marketing | Inflammatory bowel disease | Intestine | Monoclonal antibodies | Tumor necrosis factor-TNF | Remission | Colon | Endoscopy | Pharmaceutical industry | Azathioprine | Integrins
Journal Article
Infection and Immunity, ISSN 0019-9567, 05/2007, Volume 75, Issue 5, pp. 2399 - 2407
Classifications Services IAI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit...
Caco-2 Cells | Anti-Infective Agents - metabolism | Humans | Culture Media, Conditioned - chemistry | Gene Expression Regulation | Escherichia coli - immunology | Probiotics | Escherichia coli - genetics | Gene Deletion | Flagellin - chemistry | Flagellin - genetics | Flagellin - metabolism | beta-Defensins - biosynthesis | Escherichia coli - classification | Host Response and Inflammation
Caco-2 Cells | Anti-Infective Agents - metabolism | Humans | Culture Media, Conditioned - chemistry | Gene Expression Regulation | Escherichia coli - immunology | Probiotics | Escherichia coli - genetics | Gene Deletion | Flagellin - chemistry | Flagellin - genetics | Flagellin - metabolism | beta-Defensins - biosynthesis | Escherichia coli - classification | Host Response and Inflammation
Journal Article
Hepatology, ISSN 0270-9139, 04/2012, Volume 55, Issue 4, pp. 1154 - 1163
Liver cirrhosis is associated with bacterial translocation (BT) and endotoxemia. Most translocating bacteria belong to the common intestinal microbiota,...
PERITONITIS | LIVER-CIRRHOSIS | NOD2 GENE | OVERGROWTH | IN-VIVO | CHRONIC PORTAL-HYPERTENSION | ALPHA-DEFENSINS | TRANSIT-TIME | GASTROENTEROLOGY & HEPATOLOGY | ILEAL CROHNS-DISEASE | EXPRESSION | Hypertension, Portal - physiopathology | Portal Vein - physiopathology | Paneth Cells - pathology | Male | Cecum - microbiology | Rats, Inbred Strains | Liver Cirrhosis - chemically induced | Hypertension, Portal - etiology | Liver Cirrhosis - metabolism | beta-Defensins - metabolism | Bifidobacterium - physiology | Escherichia coli - physiology | Disease Models, Animal | Paneth Cells - metabolism | Bacterial Translocation - physiology | Bacteroides fragilis - physiology | Carbon Tetrachloride - adverse effects | Rats | Protein Precursors - metabolism | Animals | Intestines - microbiology | Liver Cirrhosis - pathology | Ligation - adverse effects | Ileum - microbiology | Enterococcus faecalis - physiology | Antimicrobial agents | Liver cirrhosis | Small intestine | Rodents
PERITONITIS | LIVER-CIRRHOSIS | NOD2 GENE | OVERGROWTH | IN-VIVO | CHRONIC PORTAL-HYPERTENSION | ALPHA-DEFENSINS | TRANSIT-TIME | GASTROENTEROLOGY & HEPATOLOGY | ILEAL CROHNS-DISEASE | EXPRESSION | Hypertension, Portal - physiopathology | Portal Vein - physiopathology | Paneth Cells - pathology | Male | Cecum - microbiology | Rats, Inbred Strains | Liver Cirrhosis - chemically induced | Hypertension, Portal - etiology | Liver Cirrhosis - metabolism | beta-Defensins - metabolism | Bifidobacterium - physiology | Escherichia coli - physiology | Disease Models, Animal | Paneth Cells - metabolism | Bacterial Translocation - physiology | Bacteroides fragilis - physiology | Carbon Tetrachloride - adverse effects | Rats | Protein Precursors - metabolism | Animals | Intestines - microbiology | Liver Cirrhosis - pathology | Ligation - adverse effects | Ileum - microbiology | Enterococcus faecalis - physiology | Antimicrobial agents | Liver cirrhosis | Small intestine | Rodents
Journal Article
世界胃肠病学杂志:英文版, ISSN 1007-9327, 2011, Volume 17, Issue 27, pp. 3198 - 3203
The pathogenesis of both entities of inflammatory bowel disease (IBD), namely Crohn's disease (CD) and ulcerative colitis (UC), is still complex and under...
溃疡性结肠炎 | 鸡传染性法氏囊病 | 细胞分化 | 干细胞 | 微生物菌群 | 发展中国家 | 杯状细胞 | 肠道疾病 | Hath1 | Inflammatory bowel disease | Goblet cells | Paneth cells | TCF4 | Cell differentiation | KLF4 | ULCERATIVE-COLITIS | COLON | ANTIMICROBIAL PEPTIDES | ILEAL CROHNS-DISEASE | ALPHA-DEFENSIN EXPRESSION | DIFFERENTIATION | LAYER | GASTROENTEROLOGY & HEPATOLOGY | MUCUS | INNATE IMMUNITY | Transcription Factor 4 | Humans | Inflammatory Bowel Diseases - diagnosis | Paneth Cells - pathology | Stem Cells - cytology | Transcription Factors - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Colitis, Ulcerative - diagnosis | Kruppel-Like Transcription Factors - metabolism | Inflammatory Bowel Diseases - pathology | Crohn Disease - diagnosis | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism | alpha-Defensins - metabolism | Cell Differentiation | Goblet Cells - cytology | Intestinal Mucosa - pathology | Intestines - cytology | Topic Highlight
溃疡性结肠炎 | 鸡传染性法氏囊病 | 细胞分化 | 干细胞 | 微生物菌群 | 发展中国家 | 杯状细胞 | 肠道疾病 | Hath1 | Inflammatory bowel disease | Goblet cells | Paneth cells | TCF4 | Cell differentiation | KLF4 | ULCERATIVE-COLITIS | COLON | ANTIMICROBIAL PEPTIDES | ILEAL CROHNS-DISEASE | ALPHA-DEFENSIN EXPRESSION | DIFFERENTIATION | LAYER | GASTROENTEROLOGY & HEPATOLOGY | MUCUS | INNATE IMMUNITY | Transcription Factor 4 | Humans | Inflammatory Bowel Diseases - diagnosis | Paneth Cells - pathology | Stem Cells - cytology | Transcription Factors - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Colitis, Ulcerative - diagnosis | Kruppel-Like Transcription Factors - metabolism | Inflammatory Bowel Diseases - pathology | Crohn Disease - diagnosis | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism | alpha-Defensins - metabolism | Cell Differentiation | Goblet Cells - cytology | Intestinal Mucosa - pathology | Intestines - cytology | Topic Highlight
Journal Article
EMBO Molecular Medicine, ISSN 1757-4676, 10/2013, Volume 5, Issue 10, pp. 1465 - 1483
We survive because we adapted to a world of microorganisms. All our epithelial surfaces participate in keeping up an effective barrier against microbes while...
microbiota | intestinal homeostasis | epithelial differentiation | defensin | antimicrobial peptides | Epithelial differentiation | Microbiota | Intestinal homeostasis | Defensin | Antimicrobial peptides | MEDICINE, RESEARCH & EXPERIMENTAL | CLOSTRIDIUM-DIFFICILE INFECTION | ACTIVATED RECEPTOR-GAMMA | COLI NISSLE 1917 | ILEAL CROHNS-DISEASE | ALPHA-DEFENSIN EXPRESSION | INTESTINAL EPITHELIAL-CELLS | COLONIC MUCUS BARRIER | INFLAMMATORY-BOWEL-DISEASE | TOLL-LIKE RECEPTORS | SINGLE-NUCLEOTIDE POLYMORPHISMS | Intestinal Mucosa - metabolism | Anti-Infective Agents - pharmacology | Colitis, Ulcerative - metabolism | Humans | Antimicrobial Cationic Peptides - pharmacology | Bacteria - drug effects | Crohn Disease - metabolism | Gastrointestinal Tract - microbiology | Intestinal Mucosa - microbiology | Colonic Neoplasms - metabolism | Animals | Colitis, Ulcerative - etiology | Intestinal Mucosa - immunology | Colonic Neoplasms - pathology | T-Lymphocytes - immunology | Crohn Disease - etiology | Peptides | Homeostasis | Review
microbiota | intestinal homeostasis | epithelial differentiation | defensin | antimicrobial peptides | Epithelial differentiation | Microbiota | Intestinal homeostasis | Defensin | Antimicrobial peptides | MEDICINE, RESEARCH & EXPERIMENTAL | CLOSTRIDIUM-DIFFICILE INFECTION | ACTIVATED RECEPTOR-GAMMA | COLI NISSLE 1917 | ILEAL CROHNS-DISEASE | ALPHA-DEFENSIN EXPRESSION | INTESTINAL EPITHELIAL-CELLS | COLONIC MUCUS BARRIER | INFLAMMATORY-BOWEL-DISEASE | TOLL-LIKE RECEPTORS | SINGLE-NUCLEOTIDE POLYMORPHISMS | Intestinal Mucosa - metabolism | Anti-Infective Agents - pharmacology | Colitis, Ulcerative - metabolism | Humans | Antimicrobial Cationic Peptides - pharmacology | Bacteria - drug effects | Crohn Disease - metabolism | Gastrointestinal Tract - microbiology | Intestinal Mucosa - microbiology | Colonic Neoplasms - metabolism | Animals | Colitis, Ulcerative - etiology | Intestinal Mucosa - immunology | Colonic Neoplasms - pathology | T-Lymphocytes - immunology | Crohn Disease - etiology | Peptides | Homeostasis | Review
Journal Article
Science, ISSN 0036-8075, 7/2012, Volume 337, Issue 6093, pp. 477 - 481
Defensins are antimicrobial peptides that contribute broadly to innate immunity, including protection of mucosal tissues. Human α-defensin (HD) 6 is highly...
Molecules | Epithelial cells | Transgenic animals | Biosensing techniques | Humans | REPORTS | Cell lines | Bacteria | Mice | Monomers | Vehicles | HD5 | MICE | PANETH CELLS | MULTIDISCIPLINARY SCIENCES | Intestine, Small - ultrastructure | Protein Multimerization | Immunity, Mucosal | env Gene Products, Human Immunodeficiency Virus - metabolism | Nanostructures | Salmonella Infections, Animal - immunology | Adhesins, Bacterial - metabolism | Salmonella typhimurium - ultrastructure | Macromolecular Substances - chemistry | Peptides - metabolism | Paneth Cells - immunology | Intestinal Mucosa - immunology | Protein Structure, Quaternary | Macromolecular Substances - immunology | alpha-Defensins - metabolism | Yersinia enterocolitica - immunology | Intestine, Small - immunology | Paneth Cells - metabolism | Cell Line | Microscopy, Electron, Scanning | alpha-Defensins - chemistry | Intestinal Mucosa - ultrastructure | Peptides - chemistry | Salmonella typhimurium - immunology | Salmonella typhimurium - pathogenicity | Yersinia enterocolitica - pathogenicity | Intestine, Small - microbiology | Models, Molecular | Mice, Transgenic | Intestinal Mucosa - microbiology | Immunity, Innate | Animals | alpha-Defensins - immunology | Salmonella Infections, Animal - microbiology | Protein Binding | Bacterial Proteins - metabolism | Macromolecular Substances - metabolism
Molecules | Epithelial cells | Transgenic animals | Biosensing techniques | Humans | REPORTS | Cell lines | Bacteria | Mice | Monomers | Vehicles | HD5 | MICE | PANETH CELLS | MULTIDISCIPLINARY SCIENCES | Intestine, Small - ultrastructure | Protein Multimerization | Immunity, Mucosal | env Gene Products, Human Immunodeficiency Virus - metabolism | Nanostructures | Salmonella Infections, Animal - immunology | Adhesins, Bacterial - metabolism | Salmonella typhimurium - ultrastructure | Macromolecular Substances - chemistry | Peptides - metabolism | Paneth Cells - immunology | Intestinal Mucosa - immunology | Protein Structure, Quaternary | Macromolecular Substances - immunology | alpha-Defensins - metabolism | Yersinia enterocolitica - immunology | Intestine, Small - immunology | Paneth Cells - metabolism | Cell Line | Microscopy, Electron, Scanning | alpha-Defensins - chemistry | Intestinal Mucosa - ultrastructure | Peptides - chemistry | Salmonella typhimurium - immunology | Salmonella typhimurium - pathogenicity | Yersinia enterocolitica - pathogenicity | Intestine, Small - microbiology | Models, Molecular | Mice, Transgenic | Intestinal Mucosa - microbiology | Immunity, Innate | Animals | alpha-Defensins - immunology | Salmonella Infections, Animal - microbiology | Protein Binding | Bacterial Proteins - metabolism | Macromolecular Substances - metabolism
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2005, Volume 102, Issue 50, pp. 18129 - 18134
The pathogenesis of Crohn's disease (CD), an idiopathic inflammatory bowel disease, is attributed, in part, to intestinal bacteria that may initiate and...
Biological Sciences | Inflammatory bowel diseases | Microbiota | Messenger RNA | Ileitis | Antimicrobials | Mucosa | Bacteria | Biopsies | Inflammation | Ileum | Inflammatory bowel disease | Innate immunity | Intestine | MICROFLORA | intestine | bacteria | MULTIDISCIPLINARY SCIENCES | INNATE | MECHANISMS | HUMAN INTESTINAL DEFENSIN | inflammatory bowel disease | INFLAMMATORY-BOWEL-DISEASE | PEPTIDES | innate immunity | GENE | MUTATIONS | EXPRESSION | Immunohistochemistry | Paneth Cells - metabolism | Humans | Crohn Disease - metabolism | Immunoblotting | Mice, Transgenic | Reverse Transcriptase Polymerase Chain Reaction | Crohn Disease - immunology | Animals | Analysis of Variance | Ileitis - immunology | Crohn Disease - microbiology | alpha-Defensins - metabolism | Ileitis - metabolism | Ileitis - microbiology | Mice | Ohio | Ileum - microbiology
Biological Sciences | Inflammatory bowel diseases | Microbiota | Messenger RNA | Ileitis | Antimicrobials | Mucosa | Bacteria | Biopsies | Inflammation | Ileum | Inflammatory bowel disease | Innate immunity | Intestine | MICROFLORA | intestine | bacteria | MULTIDISCIPLINARY SCIENCES | INNATE | MECHANISMS | HUMAN INTESTINAL DEFENSIN | inflammatory bowel disease | INFLAMMATORY-BOWEL-DISEASE | PEPTIDES | innate immunity | GENE | MUTATIONS | EXPRESSION | Immunohistochemistry | Paneth Cells - metabolism | Humans | Crohn Disease - metabolism | Immunoblotting | Mice, Transgenic | Reverse Transcriptase Polymerase Chain Reaction | Crohn Disease - immunology | Animals | Analysis of Variance | Ileitis - immunology | Crohn Disease - microbiology | alpha-Defensins - metabolism | Ileitis - metabolism | Ileitis - microbiology | Mice | Ohio | Ileum - microbiology
Journal Article