Research Papers:

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

Pauline Floch, Amandine Marine Laur, Victoria Korolik, Delphine Chrisment, David Cappellen, Yamina Idrissi, Pierre Dubus, Francis Mégraud and Philippe Lehours _

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Oncotarget. 2015; 6:34525-34536. https://doi.org/10.18632/oncotarget.5948

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Pauline Floch1,2,*, Amandine Marine Laur1,2,*, Victoria Korolik3, Delphine Chrisment1,2, David Cappellen4, Yamina Idrissi4, Pierre Dubus4, Francis Mégraud1,2 and Philippe Lehours1,2

1 University of Bordeaux, Bacteriology Laboratory, F-33000 Bordeaux, France

2 Inserm U853, F-33000 Bordeaux, France

3 Institute for Glycomics, Griffith University, Gold Coast, QLD, Australia

4 University of Bordeaux, EA 2406, F-33000 Bordeaux, France

* These authors have contributed equally to this work

Correspondence to:

Philippe Lehours, email:

Keywords: cytokines, chemokines, MALT lymphoma, TNF, animal model

Received: August 04, 2015 Accepted: September 08, 2015 Published: October 01, 2015


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.

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