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ali is also a major complication in severe acute pancreatitis. the pathophysiology of sap-associated ali is poorly understood, but elevated serum levels of il-6 is a reliable marker for disease severity. here, we used a mouse model of acute pancreatitis-associated (1) 1
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Journal of Clinical Investigation, ISSN 0021-9738, 03/2013, Volume 123, Issue 3, pp. 1019 - 1031
Acute lung injury (ALI) is an inflammatory disease with a high mortality rate. Although typically seen in individuals with sepsis, ALI is also a major... 
C-REACTIVE PROTEIN | INFLAMMATORY-RESPONSE | MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | Acute lung injury (ALI) is an inflammatory disease with a high mortality rate. Although typically seen in individuals with sepsis | of STAT3 and production of the neutrophil attractant CXCL1 in pancreatic acinar cells. Examination of human samples revealed expression of IL-6 in combination with soluble IL-6 receptor was a reliable predictor of ALI in SAP. These results demonstrate that IL-6 trans-signaling is an essential mediator of ALI in SAP across | INTERLEUKIN-6 | RESPIRATORY-DISTRESS-SYNDROME | PREDICTION | species and suggest that therapeutic inhibition of IL-6 may prevent SAP-associated ALI | ACUTE-PHASE RESPONSE | ALI is also a major complication in severe acute pancreatitis (SAP). The pathophysiology of SAP-associated ALI is poorly understood, but elevated serum levels of IL-6 is a reliable marker for disease severity. Here, we used a mouse model of acute pancreatitis-associated (AP-associated) ALI to determine the role of IL-6 in ALI lethality. Il6-deficient mice had a lower death rate compared with wild-type mice with AP, while mice injected with IL-6 were more likely to develop lethal ALI. We found that inflammation-associated NF-kappa B induced myeloid cell secretion of IL-6, and the effects of secreted IL-6 were mediated by complexation with soluble IL-6 receptor, a process known as trans-signaling. IL-6 trans-signaling stimulated phosphorylation | BLOCKADE | INHIBITOR | SEVERITY | Phosphorylation | Humans | NF-kappa B - metabolism | Pancreatitis - complications | Receptors, Interleukin-8B - antagonists & inhibitors | Benzenesulfonates - pharmacology | Interleukin-6 - physiology | Pancreatitis - immunology | Acute Lung Injury - metabolism | Chemokine CXCL1 - metabolism | STAT3 Transcription Factor - metabolism | Acinar Cells - metabolism | Aminosalicylic Acids - pharmacology | Signal Transduction | Mice, Inbred C57BL | Pancreas - pathology | Mice, Transgenic | Acute Lung Injury - pathology | Interleukin-6 - secretion | Animals | Myeloid Cells - secretion | Receptors, Interleukin-8B - metabolism | Myeloid Cells - metabolism | Acute Lung Injury - immunology | Pancreatitis - pathology | Mice | Phenylurea Compounds - pharmacology | Protein Processing, Post-Translational | Pancreatitis - metabolism | STAT3 Transcription Factor - antagonists & inhibitors | Acute Lung Injury - etiology | Receptors, Interleukin-6 - metabolism | Lung diseases | Pancreatitis | Genetic aspects | Research | Health aspects | Risk factors | Interleukin-6 | Index Medicus | Abridged Index Medicus | Clinical Medicine | Medical and Health Sciences | Klinisk medicin | Medicin och hälsovetenskap | Surgery | Kirurgi
Journal Article
Cell Metabolism, ISSN 1550-4131, 03/2015, Volume 21, Issue 3, pp. 493 - 501
Journal Article
Gastroenterology, ISSN 0016-5085, 2011, Volume 141, Issue 4, pp. 1473 - 1485.e7
Journal Article
Gastroenterology, ISSN 0016-5085, 2013, Volume 144, Issue 1, pp. 192 - 201
Journal Article
Gastroenterology, ISSN 0016-5085, 2016, Volume 150, Issue 2, pp. 499 - 512.e20
Background & Aims Under conditions of inflammation in the absence of micro-organisms (sterile inflammation), necrotic cells release damage-associated molecular... 
Gastroenterology and Hepatology | Immune Regulation | TLR | Cytokines | Mouse Model | ACTIVATION | MACROPHAGES | INCREASES | LUNG INJURY | DYING CELLS | IN-VIVO | ACINAR-CELLS | MICE | GASTROENTEROLOGY & HEPATOLOGY | NF-KAPPA-B | SUBUNIT | Phosphorylation | Bile Ducts - metabolism | Cholangitis, Sclerosing - prevention & control | Humans | Protein Multimerization | Transcription Factors - deficiency | Cholangitis, Sclerosing - genetics | I-kappa B Proteins - metabolism | Pancreatitis - prevention & control | Pancreatitis - genetics | Ubiquitination | Taurocholic Acid | Time Factors | Proteolysis | Bone Marrow Transplantation | Cholangitis, Sclerosing - metabolism | Proto-Oncogene Proteins - metabolism | Acute Disease | NF-KappaB Inhibitor alpha | NF-kappa B p50 Subunit - metabolism | Signal Transduction | Mice, Inbred C57BL | Pancreas - pathology | Proto-Oncogene Proteins - genetics | Pancreas - metabolism | Proto-Oncogene Proteins - deficiency | Transcription Factors - genetics | Pancreatitis - chemically induced | Mice, Knockout | Cholangitis, Sclerosing - pathology | Transcription Factors - metabolism | Animals | Transcription Factor RelA - metabolism | ATP Binding Cassette Transporter, Sub-Family B - metabolism | Pancreatitis - pathology | Pancreatitis - metabolism | Proteasome Endopeptidase Complex - metabolism | Ceruletide | ATP Binding Cassette Transporter, Sub-Family B - genetics | Bile Ducts - pathology | Analysis | Inflammation | Index Medicus | Abridged Index Medicus
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