Absence of the neutrophil serine protease cathepsin G decreases neutrophil granulocyte infiltration but does not change the severity of acute pancreatitis
Identifieur interne : 000C10 ( Ncbi/Merge ); précédent : 000C09; suivant : 000C11Absence of the neutrophil serine protease cathepsin G decreases neutrophil granulocyte infiltration but does not change the severity of acute pancreatitis
Auteurs : Ali A. Aghdassi [Allemagne] ; Daniel S. John [Allemagne] ; Matthias Sendler [Allemagne] ; Christian Storck [Allemagne] ; Cindy Van Den Brandt [Allemagne] ; Burkhard Krüger [Allemagne] ; Frank Ulrich Weiss [Allemagne] ; Julia Mayerle [Allemagne] ; Markus M. Lerch [Allemagne]Source :
- Scientific Reports [ 2045-2322 ] ; 2019.
Abstract
Acute pancreatitis is characterized by an early intracellular protease activation and invasion of leukocytes into the pancreas. Cathepsins constitute a large group of lysosomal enzymes, that have been shown to modulate trypsinogen activation and neutrophil infiltration. Cathepsin G (CTSG) is a neutrophil serine protease of the chymotrypsin C family known to degrade extracellular matrix components and to have regulatory functions in inflammatory disorders. The aim of this study was to investigate the role of CTSG in pancreatitis. Isolated acinar cells were exposed to recombinant CTSG and supramaximal cholezystokinin stimulation. In CTSG−/− mice and corresponding controls acute experimental pancreatitis was induced by serial caerulein injections. Severity was assessed by histology, serum enzyme levels and zymogen activation. Neutrophil infiltration was quantified by chloro-acetate ersterase staining and myeloperoxidase measurement. CTSG was expessed in inflammatory cells but not in pancreatic acinar cells. CTSG had no effect on intra-acinar-cell trypsinogen activation. In CTSG−/− mice a transient decrease of neutrophil infiltration into the pancreas and lungs was found during acute pancreatitis while the disease severity remained largely unchanged. CTSG is involved in pancreatic neutrophil infiltration during pancreatitis, albeit to a lesser degree than the related neutrophil (PMN) elastase. Its absence therefore leaves pancreatitis severity essentially unaffected.
Url:
DOI: 10.1038/s41598-019-53293-0
PubMed: 31727956
PubMed Central: 6856518
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PMC:6856518Le document en format XML
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<front><div type="abstract" xml:lang="en"><p id="Par1">Acute pancreatitis is characterized by an early intracellular protease activation and invasion of leukocytes into the pancreas. Cathepsins constitute a large group of lysosomal enzymes, that have been shown to modulate trypsinogen activation and neutrophil infiltration. Cathepsin G (CTSG) is a neutrophil serine protease of the chymotrypsin C family known to degrade extracellular matrix components and to have regulatory functions in inflammatory disorders. The aim of this study was to investigate the role of CTSG in pancreatitis. Isolated acinar cells were exposed to recombinant CTSG and supramaximal cholezystokinin stimulation. In CTSG<sup>−/−</sup>
mice and corresponding controls acute experimental pancreatitis was induced by serial caerulein injections. Severity was assessed by histology, serum enzyme levels and zymogen activation. Neutrophil infiltration was quantified by chloro-acetate ersterase staining and myeloperoxidase measurement. CTSG was expessed in inflammatory cells but not in pancreatic acinar cells. CTSG had no effect on intra-acinar-cell trypsinogen activation. In CTSG<sup>−/−</sup>
mice a transient decrease of neutrophil infiltration into the pancreas and lungs was found during acute pancreatitis while the disease severity remained largely unchanged. CTSG is involved in pancreatic neutrophil infiltration during pancreatitis, albeit to a lesser degree than the related neutrophil (PMN) elastase. Its absence therefore leaves pancreatitis severity essentially unaffected.</p>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Sci Rep</journal-id>
<journal-id journal-id-type="iso-abbrev">Sci Rep</journal-id>
<journal-title-group><journal-title>Scientific Reports</journal-title>
</journal-title-group>
<issn pub-type="epub">2045-2322</issn>
<publisher><publisher-name>Nature Publishing Group UK</publisher-name>
<publisher-loc>London</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31727956</article-id>
<article-id pub-id-type="pmc">6856518</article-id>
<article-id pub-id-type="publisher-id">53293</article-id>
<article-id pub-id-type="doi">10.1038/s41598-019-53293-0</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Absence of the neutrophil serine protease cathepsin G decreases neutrophil granulocyte infiltration but does not change the severity of acute pancreatitis</article-title>
</title-group>
<contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">http://orcid.org/0000-0002-0569-7316</contrib-id>
<name><surname>Aghdassi</surname>
<given-names>Ali A.</given-names>
</name>
<address><email>aghdassi@uni-greifswald.de</email>
</address>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>John</surname>
<given-names>Daniel S.</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sendler</surname>
<given-names>Matthias</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Storck</surname>
<given-names>Christian</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>van den Brandt</surname>
<given-names>Cindy</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Krüger</surname>
<given-names>Burkhard</given-names>
</name>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Weiss</surname>
<given-names>Frank Ulrich</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Mayerle</surname>
<given-names>Julia</given-names>
</name>
<xref ref-type="aff" rid="Aff3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lerch</surname>
<given-names>Markus M.</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<aff id="Aff1"><label>1</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.5603.0</institution-id>
<institution>Department of Medicine A,</institution>
<institution>University Medicine Greifswald,</institution>
</institution-wrap>
17475 Greifswald, Germany</aff>
<aff id="Aff2"><label>2</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000000121858338</institution-id>
<institution-id institution-id-type="GRID">grid.10493.3f</institution-id>
<institution>Division of Medical Biology,</institution>
<institution>University of Rostock,</institution>
</institution-wrap>
18051 Rostock, Germany</aff>
<aff id="Aff3"><label>3</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1936 973X</institution-id>
<institution-id institution-id-type="GRID">grid.5252.0</institution-id>
<institution>Department of Medicine II,</institution>
<institution>Ludwigs-Maximilians University Munich,</institution>
</institution-wrap>
80539 Munich, Germany</aff>
</contrib-group>
<pub-date pub-type="epub"><day>14</day>
<month>11</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>14</day>
<month>11</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>9</volume>
<elocation-id>16774</elocation-id>
<history><date date-type="received"><day>18</day>
<month>7</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>30</day>
<month>10</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© The Author(s) 2019</copyright-statement>
<license license-type="OpenAccess"><license-p><bold>Open Access</bold>
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>
.</license-p>
</license>
</permissions>
<abstract id="Abs1"><p id="Par1">Acute pancreatitis is characterized by an early intracellular protease activation and invasion of leukocytes into the pancreas. Cathepsins constitute a large group of lysosomal enzymes, that have been shown to modulate trypsinogen activation and neutrophil infiltration. Cathepsin G (CTSG) is a neutrophil serine protease of the chymotrypsin C family known to degrade extracellular matrix components and to have regulatory functions in inflammatory disorders. The aim of this study was to investigate the role of CTSG in pancreatitis. Isolated acinar cells were exposed to recombinant CTSG and supramaximal cholezystokinin stimulation. In CTSG<sup>−/−</sup>
mice and corresponding controls acute experimental pancreatitis was induced by serial caerulein injections. Severity was assessed by histology, serum enzyme levels and zymogen activation. Neutrophil infiltration was quantified by chloro-acetate ersterase staining and myeloperoxidase measurement. CTSG was expessed in inflammatory cells but not in pancreatic acinar cells. CTSG had no effect on intra-acinar-cell trypsinogen activation. In CTSG<sup>−/−</sup>
mice a transient decrease of neutrophil infiltration into the pancreas and lungs was found during acute pancreatitis while the disease severity remained largely unchanged. CTSG is involved in pancreatic neutrophil infiltration during pancreatitis, albeit to a lesser degree than the related neutrophil (PMN) elastase. Its absence therefore leaves pancreatitis severity essentially unaffected.</p>
</abstract>
<kwd-group kwd-group-type="npg-subject"><title>Subject terms</title>
<kwd>Acute pancreatitis</kwd>
<kwd>Health sciences</kwd>
</kwd-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/501100001659</institution-id>
<institution>Deutsche Forschungsgemeinschaft (German Research Foundation)</institution>
</institution-wrap>
</funding-source>
<award-id>SE 2702/2-1</award-id>
<award-id>MA 4115/1-2/3</award-id>
<award-id>GRK 1947;A3</award-id>
<principal-award-recipient><name><surname>Sendler</surname>
<given-names>Matthias</given-names>
</name>
<name><surname>Mayerle</surname>
<given-names>Julia</given-names>
</name>
<name><surname>Lerch</surname>
<given-names>Markus M.</given-names>
</name>
</principal-award-recipient>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/501100004895</institution-id>
<institution>EC | Directorate-General for Employment, Social Affairs and Inclusion | European Social Fund (Fondo Social Europeo)</institution>
</institution-wrap>
</funding-source>
<award-id>ESF/14-BM-A55-0045/16</award-id>
<award-id>ESF/14-BM-A55-0045/16</award-id>
<award-id>ESF/14-BM-A55-0045/16 and ESF/14-BM-A55-0008/18</award-id>
<principal-award-recipient><name><surname>Weiss</surname>
<given-names>Frank Ulrich</given-names>
</name>
<name><surname>Mayerle</surname>
<given-names>Julia</given-names>
</name>
<name><surname>Lerch</surname>
<given-names>Markus M.</given-names>
</name>
</principal-award-recipient>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/100010661</institution-id>
<institution>EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)</institution>
</institution-wrap>
</funding-source>
<award-id>EU-FP-7: EPC-TM</award-id>
<award-id>EU-FP-7: EPC-TM</award-id>
<principal-award-recipient><name><surname>Mayerle</surname>
<given-names>Julia</given-names>
</name>
<name><surname>Lerch</surname>
<given-names>Markus M.</given-names>
</name>
</principal-award-recipient>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/501100002347</institution-id>
<institution>Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research)</institution>
</institution-wrap>
</funding-source>
<award-id>BMBF GANI-MED 03IS2061A, BMBF 0314107, 01ZZ9603, 01ZZ0103, 01ZZ0403, 03ZIK012, 03zz0921E</award-id>
<award-id>BMBF GANI-MED 03IS2061A and BMBF 0314107, 01ZZ9603, 01ZZ0103, 01ZZ0403, 03ZIK012, 03zz0921E</award-id>
<principal-award-recipient><name><surname>Mayerle</surname>
<given-names>Julia</given-names>
</name>
<name><surname>Lerch</surname>
<given-names>Markus M.</given-names>
</name>
</principal-award-recipient>
</award-group>
</funding-group>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© The Author(s) 2019</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>Allemagne</li>
</country>
</list>
<tree><country name="Allemagne"><noRegion><name sortKey="Aghdassi, Ali A" sort="Aghdassi, Ali A" uniqKey="Aghdassi A" first="Ali A." last="Aghdassi">Ali A. Aghdassi</name>
</noRegion>
<name sortKey="John, Daniel S" sort="John, Daniel S" uniqKey="John D" first="Daniel S." last="John">Daniel S. John</name>
<name sortKey="Kruger, Burkhard" sort="Kruger, Burkhard" uniqKey="Kruger B" first="Burkhard" last="Krüger">Burkhard Krüger</name>
<name sortKey="Lerch, Markus M" sort="Lerch, Markus M" uniqKey="Lerch M" first="Markus M." last="Lerch">Markus M. Lerch</name>
<name sortKey="Mayerle, Julia" sort="Mayerle, Julia" uniqKey="Mayerle J" first="Julia" last="Mayerle">Julia Mayerle</name>
<name sortKey="Sendler, Matthias" sort="Sendler, Matthias" uniqKey="Sendler M" first="Matthias" last="Sendler">Matthias Sendler</name>
<name sortKey="Storck, Christian" sort="Storck, Christian" uniqKey="Storck C" first="Christian" last="Storck">Christian Storck</name>
<name sortKey="Van Den Brandt, Cindy" sort="Van Den Brandt, Cindy" uniqKey="Van Den Brandt C" first="Cindy" last="Van Den Brandt">Cindy Van Den Brandt</name>
<name sortKey="Weiss, Frank Ulrich" sort="Weiss, Frank Ulrich" uniqKey="Weiss F" first="Frank Ulrich" last="Weiss">Frank Ulrich Weiss</name>
</country>
</tree>
</affiliations>
</record>
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