The discovery, reported by the Howard Hughes Medical Institute, explains how Listeria monocytogenes, a common food-borne pathogen, invades cells and avoids the body’s immune system. The research by Pascale Cossart, a Howard Hughes Medical Institute international research scholar, and her colleague Esteban Veiga at the Institut Pasteur in Paris was published yesterday in Nature Cell Biology. From the press release:
Cossart’s lab had observed that Listeria – which is 20 times the size of the largest particle scientists believed a cell could take in by endocytosis – could invade non-phagocytic cells. Other labs had made similar observations with other bacteria. Cossart and Veiga investigated the underlying machinery behind this uncommon invasion strategy, which they knew depended on an interaction between a protein on the surface of the bacteria, known as InlB, and a protein called Met on the surface of the cell it was invading.
They discovered that when InlB interacts with Met, the cell responds by adding a chemical tag to Met that flags it for protein recycling or degradation. Since Met is on the outside surface of the cell and the recycling and degradation machineries are inside, the cell must bring Met inside through endocytosis in order to dispose of it. As the cell creates the vesicle that will transport tagged Met, Listeria stows away and invades the cell.
By manipulating the gene expression of the cells Listeria was invading, the researchers showed that specific molecules known to be involved in endocytosis were essential for successful invasion by Listeria. Similarly, they found that an enzyme that tags proteins for recycling was also required.
Listeria’s use of receptor-mediated endocytosis to infect hosts, according to Cossart, suggests that other bacteria may exploit the same mechanism to gain entry into non-phagocytic cells.
The press release…