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Peptic ulcer bacterium alters the body's defence system

30.06.2009
Helicobacter pylori survives in the body by manipulating important immune system cells. This is shown in a thesis from the Sahlgrenska Academy, University of Gothenburg, Sweden. The discovery may lead to new treatments against the common peptic ulcer bacterium.

About half of the world's population carries Helicobacter pylori, mainly in the stomach. Most infected individuals never experience any symptoms, but around 10% get peptic ulcers and around 1% develop stomach cancer.

'Carriers were often infected as children and if not treated with antibiotics, the bacterium remains in the body for life. The immune system alone is unable to eliminate the bacterium, and now we understand better why', says biologist Bert Kindlund, the author of the thesis.

The study shows that a type of cells in the immune system called regulatory T cells down-regulate the body's defence against Helicobacter pylori and thereby enable the bacterium to develop a chronic infection. 'If we could control the regulatory T cells, we could strengthen the immune system and help the body eliminate the bacterium. This could be a new treatment strategy against Helicobacter pylori', Kindlund continues.

In addition, the bacterium makes the immune system increase the number of regulatory T cells in the lining of the stomach. This also occurs with stomach cancer. 'An important question is where the increased number of regulatory T cells in the stomach lining come from. Knowing the answer to this question could help us develop a treatment for stomach cancer. What we have found so far is that the regulatory T cells are actively recruited from the bloodstream into the tumour, and once there they start multiplying faster', says Kindlund.

For more information please contact:
Bert Kindlund, biologist, telephone +46 (0)73 535 49 96, e-mail bert.kindlund@microbio.gu.se
Supervisors:
Samuel Lundin, Associate Professor, telephone +46 (0)31 786 6207, e-mail samuel.lundin@microbio.gu.se

Åsa Sjöling, Associate Professor, telephone +46 (0)31 786 62 32, e-mail asa.sjoling@microbio.gu.se

A thesis presented for the degree of Doctor of Philosophy (Medicine) at the Sahlgrenska Academy, Institute of Biomedicine, Department of Microbiology and Immunology.

The thesis is based on the following papers:
I. Bert Kindlund, Åsa Sjöling, Malin Hansson, Anders Edebo, Lars-Erik Hansson, Henrik Sjövall, Ann-Mari Svennerholm and B. Samuel Lundin
FOXP3-expressing CD4+ T-cell numbers increase in areas of duodenal gastric metaplasia and are associated to CD4+ T-cell aggregates in the duodenum of Helicobacter pylori-infected duodenal ulcer patients. Helicobacter 2009 June; 14 (3): 192-201
II. Karin Enarsson, Anna Lundgren, Bert Kindlund, Mikael Hermansson, Giovanna Roncador, Alison H Banham, B. Samuel Lundin and Marianne Quiding-Järbrink
Function and recruitment of mucosal regulatory T cells in human chronic Helicobacter pylori infection and gastric adenocarcinoma. Clin Immunol 2006 Dec; 121 (3): 358-68
III. B. Samuel Lundin, Karin Enarsson, Bert Kindlund, Anna Lundgren, Erik Johnsson, Marianne Quiding-Järbrink and Ann-Mari Svennerholm

The local and systemic T-cell response to Helicobacter pylori in gastric cancer patients is characterised by production of interleukin-10. Clin Immunol 2007 Nov; 125 (2) 205-13

Helena Aaberg | idw
Further information:
http://www.gu.se/

Further reports about: CD4+ Helicobacter pylori Peptic T cells T-cell immune system stomach cancer

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