The author has kindly provided an example of a Lay abstract for this manuscript:
Lay Abstract
Human infections with the bacterium Helicobacter pylori are closely connected with severe inflammation and stomach ulcers, which can develop into gastric cancers. Therefore, H. pylori was the first bacterial pathogen classified as a carcinogen by the WHO. Today, gastric cancers are the second leading cause of cancer-related deaths worldwide which is mainly due to their high tendency to quickly spread throughout the body (metastasis). H. pylori can induce the motility of infected cells, resembling the metastasizing phenotype of tumor cells. In this review we summarize the existing information on the intracellular processes controlling the migration of H. pylori-infected cells. We provide an overview on the regulation of a microscopic skeleton that is found in most cells (cytoskeleton) which is built by contractile fibers composed of the protein actin. There are mainly two signal transmission routes switched on by H. pylori binding which lead to the regulation of the actin cytoskeleton. H. pylori can assemble a syringe-like structure, which injects the bacterial protein CagA into the host cell where it interferes with signals leading the drastic changes in cell shape (signal route 1). The second signal is generated by the interaction of the injection syringe itself with a family of cell surface proteins known as the integrin receptor family (signal route 2). This signal branches into a multitude of additional signaling routes that alter the actin cytoskeleton, thereby allowing cell motility. Understanding the details of such signals, how they are regulated and how they work together, could eventually lead to new approaches for treating bacterial infections as well as stomach cancers.
Cell Communication and Signaling
Lay abstract
11 April 2012
The author has kindly provided an example of a Lay abstract for this manuscript:
Lay Abstract
Human infections with the bacterium Helicobacter pylori are closely connected with severe inflammation and stomach ulcers, which can develop into gastric cancers. Therefore, H. pylori was the first bacterial pathogen classified as a carcinogen by the WHO. Today, gastric cancers are the second leading cause of cancer-related deaths worldwide which is mainly due to their high tendency to quickly spread throughout the body (metastasis). H. pylori can induce the motility of infected cells, resembling the metastasizing phenotype of tumor cells. In this review we summarize the existing information on the intracellular processes controlling the migration of H. pylori-infected cells. We provide an overview on the regulation of a microscopic skeleton that is found in most cells (cytoskeleton) which is built by contractile fibers composed of the protein actin. There are mainly two signal transmission routes switched on by H. pylori binding which lead to the regulation of the actin cytoskeleton. H. pylori can assemble a syringe-like structure, which injects the bacterial protein CagA into the host cell where it interferes with signals leading the drastic changes in cell shape (signal route 1). The second signal is generated by the interaction of the injection syringe itself with a family of cell surface proteins known as the integrin receptor family (signal route 2). This signal branches into a multitude of additional signaling routes that alter the actin cytoskeleton, thereby allowing cell motility. Understanding the details of such signals, how they are regulated and how they work together, could eventually lead to new approaches for treating bacterial infections as well as stomach cancers.
Competing interests
None declared