May 27, 2008 For the first time researchers from Australia and The Netherlands examine the inflammatory response induced by macrophages that may contribute to the development of gastritis during Helicobacter pylori infection in mice.
H. pylori is the causative agent of human chronic gastritis, a condition that often leads to gastrointestinal ulcers and cancer. The gastric mucus found in the human stomach of a H. pylori infection-free adult or child is populated by very few macrophages, however previous research shows that macrophages increase in number in response to H. pylori infection. The mouse model of Helicobacter infection mimics human H. pylori disease in many ways and offers researchers an opportunity to analyze the adaptive immune regulation of Helicobacter-induced chronic gastritis.
Macrophages are defined as white blood cells that are key players in the immune response to foreign invaders. In the study mice were intravenously injected with drug-loaded liposomes to deliberately deplete their spleens and stomachs of macrophages and then infected with H. pylori. Results showed that elimination of macrophages reduced the gastric pathology induced by H. pylori, however it did not affect bacterial presence in the stomach.
"This study demonstrates that macrophages have a central role in Helicobacter infection-induced gastritis but do not affect H. pylori-specific antibody responses," say the researchers. "In identifying a role for macrophages in the initiation of gastritis during H. pylori infection, this study may assist in future studies targeting the inhibition of gastritis in the host and provide a stimulus to study the capacity of macrophage-modifying drugs to reduce the gastritis associated with Helicobacter disease.
Other social bookmarking and sharing tools:
- M. Kaparakis, A.K. Walduck, J.D. Price, J.S. Pedersen, N. van Rooijen, M.J. Pearse, O.L.C. Wijburg, R.A. Strugnell. 2008. Macrophages are mediators of gastritis in acute Helicobacter pylori infection in C57BL/6 mice. Infection and Immunity, 76. 5: 2235-2239. doi:10.1128/IAI.01481-07
Note: If no author is given, the source is cited instead.