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

Identifieur interne : 003059 ( Main/Exploration ); précédent : 003058; suivant : 003060

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

Descripteurs français

English descriptors

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


Affiliations:


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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>
</div>
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<li>France</li>
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<name sortKey="Cappellen, David" sort="Cappellen, David" uniqKey="Cappellen D" first="David" last="Cappellen">David Cappellen</name>
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<name sortKey="Lehours, Philippe" sort="Lehours, Philippe" uniqKey="Lehours P" first="Philippe" last="Lehours">Philippe Lehours</name>
<name sortKey="Megraud, Francis" sort="Megraud, Francis" uniqKey="Megraud F" first="Francis" last="Mégraud">Francis Mégraud</name>
<name sortKey="Megraud, Francis" sort="Megraud, Francis" uniqKey="Megraud F" first="Francis" last="Mégraud">Francis Mégraud</name>
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