Approximately half of the world's population are infected with Helicobacter pylori, found primarily in the stomach. The majority never show any symptoms, but just over ten per cent develop gastric ulcers, while around one per cent develop gastric adenocarcinoma. Without antibiotics the body is unable to rid itself of the bacteria.
"Helicobacter pylori inhibits our immune defence, preventing it from attacking the bacteria with sufficient strength, despite an immune response being activated," says biologist Malin Hansson, the author of the thesis.
When an immune response is initiated a specific type of cell migrates to the lymph nodes to activate new immune cells, telling them where they need to go to tackle the infection. Infection with Helicobacter pylori prevents many of these cells from reaching their intended destination.
"Helicobacter pylori causes immune cells to accumulate in tissue. Many of the cells that ought to collect more new immune cells stop at these accumulations and begin activating these instead, leading to chronic inflammation, which we believe benefits Helicobacter pylori," says Malin Hansson.
This thesis also paves the way for a future vaccine against gastric adenocarcinoma. Previous research has shown that many infected patients with gastric adenocarcinoma have low levels of a specific type of antibody in tissue, even though Helicobacter pylori normally causes unusually high levels of antibodies. These antibodies should therefore be able to protect against this form of cancer. For the first time in samples taken from humans Malin Hansson has been able to show that these antibodies are attracted to tissue by a signal substance called MEC.
"If these antibodies really can protect against development of gastric adenocarcinoma, it would be possible to develop a vaccine that increases MEC expression and thus the number of antibodies present in tissue," says Malin.
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Enzymes behave differently in a test tube compared with the molecular scrum of a living cell. Chemists from the University of Basel have now been able to...
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