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Characterisation of inflammatory processes in Helicobacter pylori-induced gastric lymphomagenesis in a mouse model

Identifieur interne : 000569 ( Pmc/Curation ); précédent : 000568; suivant : 000570

Characterisation of inflammatory processes in Helicobacter pylori-induced gastric lymphomagenesis in a mouse model

Auteurs : Pauline Floch [France] ; Amandine Marine Laur [France] ; Victoria Korolik [Australie] ; Delphine Chrisment [France] ; David Cappellen [France] ; Yamina Idrissi [France] ; Pierre Dubus [France] ; Francis Mégraud [France] ; Philippe Lehours [France]

Source :

RBID : PMC:4741470

Abstract

Gastric MALT lymphoma (GML) can be induced by Helicobacter pylori infection in BALB/c mice thymectomised at day 3 post-birth (d3Tx). This represented a unique opportunity to investigate the inflammatory process involved in the recruitment, proliferation and structuration of lymphoid infiltrates in the gastric mucosa of mice developing GML. Complementary molecular and proteomic approaches demonstrated that Th1 and Th2 cytokines were upregulated, along with activators/regulators of the lymphoid response and numerous chemokines. Interleukin-4, interferon γ, lymphotoxin-α and -β were significantly upregulated and correlated with the inflammatory scores for all the d3Tx mice. GML lesions in d3Tx mice infected with H. pylori were associated with the presence of the inflammatory response. The dysregulation of numerous members of the tumour necrosis factor superfamily was also evident and suggests that they could play an important role in GML pathology, especially in light of their ability to promote and control lymphocyte proliferation.


Url:
PubMed: 26439692
PubMed Central: 4741470

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PMC:4741470

Le document en format XML

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<p>Gastric MALT lymphoma (GML) can be induced by
<italic>Helicobacter pylori</italic>
infection in BALB/c mice thymectomised at day 3 post-birth (d3Tx). This represented a unique opportunity to investigate the inflammatory process involved in the recruitment, proliferation and structuration of lymphoid infiltrates in the gastric mucosa of mice developing GML. Complementary molecular and proteomic approaches demonstrated that Th1 and Th2 cytokines were upregulated, along with activators/regulators of the lymphoid response and numerous chemokines. Interleukin-4, interferon γ, lymphotoxin-α and -β were significantly upregulated and correlated with the inflammatory scores for all the d3Tx mice. GML lesions in d3Tx mice infected with
<italic>H. pylori</italic>
were associated with the presence of the inflammatory response. The dysregulation of numerous members of the tumour necrosis factor superfamily was also evident and suggests that they could play an important role in GML pathology, especially in light of their ability to promote and control lymphocyte proliferation.</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">Oncotarget</journal-id>
<journal-id journal-id-type="iso-abbrev">Oncotarget</journal-id>
<journal-id journal-id-type="publisher-id">ImpactJ</journal-id>
<journal-title-group>
<journal-title>Oncotarget</journal-title>
</journal-title-group>
<issn pub-type="epub">1949-2553</issn>
<publisher>
<publisher-name>Impact Journals LLC</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">26439692</article-id>
<article-id pub-id-type="pmc">4741470</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Research Paper</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Characterisation of inflammatory processes in
<italic>Helicobacter pylori</italic>
-induced gastric lymphomagenesis in a mouse model</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" equal-contrib="yes">
<name>
<surname>Floch</surname>
<given-names>Pauline</given-names>
</name>
<xref ref-type="aff" rid="A1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="A2">
<sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author" equal-contrib="yes">
<name>
<surname>Laur</surname>
<given-names>Amandine Marine</given-names>
</name>
<xref ref-type="aff" rid="A1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="A2">
<sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Korolik</surname>
<given-names>Victoria</given-names>
</name>
<xref ref-type="aff" rid="A3">
<sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Chrisment</surname>
<given-names>Delphine</given-names>
</name>
<xref ref-type="aff" rid="A1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="A2">
<sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Cappellen</surname>
<given-names>David</given-names>
</name>
<xref ref-type="aff" rid="A4">
<sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Idrissi</surname>
<given-names>Yamina</given-names>
</name>
<xref ref-type="aff" rid="A4">
<sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Dubus</surname>
<given-names>Pierre</given-names>
</name>
<xref ref-type="aff" rid="A4">
<sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Mégraud</surname>
<given-names>Francis</given-names>
</name>
<xref ref-type="aff" rid="A1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="A2">
<sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Lehours</surname>
<given-names>Philippe</given-names>
</name>
<xref ref-type="aff" rid="A1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="A2">
<sup>2</sup>
</xref>
</contrib>
</contrib-group>
<aff id="A1">
<sup>1</sup>
University of Bordeaux, Bacteriology Laboratory, F-33000 Bordeaux, France</aff>
<aff id="A2">
<sup>2</sup>
Inserm U853, F-33000 Bordeaux, France</aff>
<aff id="A3">
<sup>3</sup>
Institute for Glycomics, Griffith University, Gold Coast, QLD, Australia</aff>
<aff id="A4">
<sup>4</sup>
University of Bordeaux, EA 2406, F-33000 Bordeaux, France</aff>
<author-notes>
<corresp id="cor1">
<bold>
<italic>Correspondence to:</italic>
</bold>
<italic>Philippe Lehours,</italic>
<email>philippe.lehours@u-bordeaux.fr</email>
</corresp>
</author-notes>
<pub-date pub-type="collection">
<day>27</day>
<month>10</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub">
<day>1</day>
<month>10</month>
<year>2015</year>
</pub-date>
<volume>6</volume>
<issue>33</issue>
<fpage>34525</fpage>
<lpage>34536</lpage>
<history>
<date date-type="received">
<day>4</day>
<month>8</month>
<year>2015</year>
</date>
<date date-type="accepted">
<day>8</day>
<month>9</month>
<year>2015</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright: © 2015 Floch et al.</copyright-statement>
<copyright-year>2015</copyright-year>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/2.5/">
<license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</license-p>
</license>
</permissions>
<abstract>
<p>Gastric MALT lymphoma (GML) can be induced by
<italic>Helicobacter pylori</italic>
infection in BALB/c mice thymectomised at day 3 post-birth (d3Tx). This represented a unique opportunity to investigate the inflammatory process involved in the recruitment, proliferation and structuration of lymphoid infiltrates in the gastric mucosa of mice developing GML. Complementary molecular and proteomic approaches demonstrated that Th1 and Th2 cytokines were upregulated, along with activators/regulators of the lymphoid response and numerous chemokines. Interleukin-4, interferon γ, lymphotoxin-α and -β were significantly upregulated and correlated with the inflammatory scores for all the d3Tx mice. GML lesions in d3Tx mice infected with
<italic>H. pylori</italic>
were associated with the presence of the inflammatory response. The dysregulation of numerous members of the tumour necrosis factor superfamily was also evident and suggests that they could play an important role in GML pathology, especially in light of their ability to promote and control lymphocyte proliferation.</p>
</abstract>
<kwd-group>
<kwd>cytokines</kwd>
<kwd>chemokines</kwd>
<kwd>MALT lymphoma</kwd>
<kwd>TNF</kwd>
<kwd>animal model</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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