UnivTrevesV1, PubMed, Corpus, bibRecord, 000158

Externalized decondensed neutrophil chromatin occludes pancreatic ducts and drives pancreatitis.

Identifieur interne : 000158 ( PubMed/Corpus ); précédent : 000157; suivant : 000159

Externalized decondensed neutrophil chromatin occludes pancreatic ducts and drives pancreatitis.

Auteurs : Moritz Leppkes ; Christian Maueröder ; Sebastian Hirth ; Stefanie Nowecki ; Claudia Günther ; Ulrike Billmeier ; Susanne Paulus ; Mona Biermann ; Luis E. Munoz ; Markus Hoffmann ; Dane Wildner ; Andrew L. Croxford ; Ari Waisman ; Kerri Mowen ; Dieter E. Jenne ; Veit Krenn ; Julia Mayerle ; Markus M. Lerch ; Georg Schett ; Stefan Wirtz ; Markus F. Neurath ; Martin Herrmann ; Christoph Becker

Source :

Nature communications [ 2041-1723 ] ; 2016.

RBID : pubmed:26964500

English descriptors

KwdEn :
- Animals, Ceruletide (toxicity), Chromatin (immunology), Cytokines (immunology), Disease Models, Animal, Extracellular Traps (immunology), Flow Cytometry, Humans, Hydrolases (metabolism), Immunohistochemistry, Interleukin-17 (pharmacology), Mice, Neutrophils (immunology), Pancreas (drug effects), Pancreas (immunology), Pancreas (pathology), Pancreatic Ducts (immunology), Pancreatic Ducts (pathology), Pancreatic Juice (enzymology), Pancreatic Juice (immunology), Pancreatitis (chemically induced), Pancreatitis (immunology), Pancreatitis (pathology), Reverse Transcriptase Polymerase Chain Reaction.
MESH :
- chemical , immunology : Chromatin, Cytokines.
- chemical , metabolism : Hydrolases.
- chemical , pharmacology : Interleukin-17.
- chemical , toxicity : Ceruletide.
- chemically induced : Pancreatitis.
- drug effects : Pancreas.
- enzymology : Pancreatic Juice.
- immunology : Extracellular Traps, Neutrophils, Pancreas, Pancreatic Ducts, Pancreatic Juice, Pancreatitis.
- pathology : Pancreas, Pancreatic Ducts, Pancreatitis.
- Animals, Disease Models, Animal, Flow Cytometry, Humans, Immunohistochemistry, Mice, Reverse Transcriptase Polymerase Chain Reaction.

Abstract

Ductal occlusion has been postulated to precipitate focal pancreatic inflammation, while the nature of the primary occluding agents has remained elusive. Neutrophils make use of histone citrullination by peptidyl arginine deiminase-4 (PADI4) in contact to particulate agents to extrude decondensed chromatin as neutrophil extracellular traps (NETs). In high cellular density, NETs form macroscopically visible aggregates. Here we show that such aggregates form inside pancreatic ducts in humans and mice occluding pancreatic ducts and thereby driving pancreatic inflammation. Experimental models indicate that PADI4 is critical for intraductal aggregate formation and that PADI4-deficiency abrogates disease progression. Mechanistically, we identify the pancreatic juice as a strong instigator of neutrophil chromatin extrusion. Characteristic single components of pancreatic juice, such as bicarbonate ions and calcium carbonate crystals, induce aggregated NET formation. Ductal occlusion by aggregated NETs emerges as a pathomechanism with relevance in a plethora of inflammatory conditions involving secretory ducts.

DOI: 10.1038/ncomms10973
PubMed: 26964500

Links to Exploration step

pubmed:26964500

Le document en format XML

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<author><name sortKey="Maueroder, Christian" sort="Maueroder, Christian" uniqKey="Maueroder C" first="Christian" last="Maueröder">Christian Maueröder</name>
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<term>Disease Models, Animal</term>
<term>Extracellular Traps (immunology)</term>
<term>Flow Cytometry</term>
<term>Humans</term>
<term>Hydrolases (metabolism)</term>
<term>Immunohistochemistry</term>
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<term>Pancreatitis (immunology)</term>
<term>Pancreatitis (pathology)</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
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<front><div type="abstract" xml:lang="en">Ductal occlusion has been postulated to precipitate focal pancreatic inflammation, while the nature of the primary occluding agents has remained elusive. Neutrophils make use of histone citrullination by peptidyl arginine deiminase-4 (PADI4) in contact to particulate agents to extrude decondensed chromatin as neutrophil extracellular traps (NETs). In high cellular density, NETs form macroscopically visible aggregates. Here we show that such aggregates form inside pancreatic ducts in humans and mice occluding pancreatic ducts and thereby driving pancreatic inflammation. Experimental models indicate that PADI4 is critical for intraductal aggregate formation and that PADI4-deficiency abrogates disease progression. Mechanistically, we identify the pancreatic juice as a strong instigator of neutrophil chromatin extrusion. Characteristic single components of pancreatic juice, such as bicarbonate ions and calcium carbonate crystals, induce aggregated NET formation. Ductal occlusion by aggregated NETs emerges as a pathomechanism with relevance in a plethora of inflammatory conditions involving secretory ducts.</div>
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<Day>11</Day>
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<DateCompleted><Year>2016</Year>
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<Title>Nature communications</Title>
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<ArticleTitle>Externalized decondensed neutrophil chromatin occludes pancreatic ducts and drives pancreatitis.</ArticleTitle>
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<Abstract><AbstractText>Ductal occlusion has been postulated to precipitate focal pancreatic inflammation, while the nature of the primary occluding agents has remained elusive. Neutrophils make use of histone citrullination by peptidyl arginine deiminase-4 (PADI4) in contact to particulate agents to extrude decondensed chromatin as neutrophil extracellular traps (NETs). In high cellular density, NETs form macroscopically visible aggregates. Here we show that such aggregates form inside pancreatic ducts in humans and mice occluding pancreatic ducts and thereby driving pancreatic inflammation. Experimental models indicate that PADI4 is critical for intraductal aggregate formation and that PADI4-deficiency abrogates disease progression. Mechanistically, we identify the pancreatic juice as a strong instigator of neutrophil chromatin extrusion. Characteristic single components of pancreatic juice, such as bicarbonate ions and calcium carbonate crystals, induce aggregated NET formation. Ductal occlusion by aggregated NETs emerges as a pathomechanism with relevance in a plethora of inflammatory conditions involving secretory ducts.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Leppkes</LastName>
<ForeName>Moritz</ForeName>
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<AffiliationInfo><Affiliation>Department of Medicine 1, University Clinics Erlangen, University of Erlangen-Nuremberg, 91054 Erlangen, Germany.</Affiliation>
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<Author ValidYN="Y"><LastName>Maueröder</LastName>
<ForeName>Christian</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Medicine 3, University Clinics Erlangen, University of Erlangen-Nuremberg, 91054 Erlangen, Germany.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Hirth</LastName>
<ForeName>Sebastian</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Institute of Molecular Medicine, University Medicine of Johannes Gutenberg University, 55131 Mainz, Germany.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Nowecki</LastName>
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   |texte=   Externalized decondensed neutrophil chromatin occludes pancreatic ducts and drives pancreatitis.
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Externalized decondensed neutrophil chromatin occludes pancreatic ducts and drives pancreatitis.

Externalized decondensed neutrophil chromatin occludes pancreatic ducts and drives pancreatitis.

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