Yale Researchers Reveal How Fresh Water Bacteria That Cause Legionnaire's Disease, Take Hold in Cells

Yale researchers have revealed how a kind of bacterium that causes Legionnaire's disease can navigate its own course within a human cell by injecting a protein that can steer host cell membranes.

Yale researchers have revealed how a kind of bacterium that causes Legionnaire’s disease can navigate its own course within a human cell by injecting a protein that can steer host cell membranes.

Legionnaire’s disease is a severe pneumonia resulting from an infection by the bacteria Legionella pneumophila. The bacteria are present in freshwater environments where they grow inside amoebae. When drops of water containing Legionella are inhaled by humans, these bacteria gain access to the lung and will grow inside the alveolar macrophages, which are specialized cells that usually destroy bacteria that have invaded the body.

“These results show that the Legionella bacteria have the ability to inject a bacterial protein directly into macrophages during infection,” said the study’s senior author Craig Roy, associate professor of microbial pathogenesis at Yale School of Medicine.

The article, published in the January 25 issue of Science, showed that the reason Legionella can survive after being ingested by macrophages is that these bacteria can prevent the membrane-bound compartment in which they reside from being transported to lysosomes, which are the compartments containing degradative enzymes that will destroy most bacteria internalized by macrophages. Rather than being transported to lysosomes, compartments containing Legionella are transported to the endoplasmic reticulum, which is a nutrient-rich compartment that supports replication of Legionella within the macrophage.

Roy said the bacteria are being delivered to a location in the host cell where bacteria are not intended to reside, and one of the proteins Legionella uses functions identically and was most likely stolen from a host cell.

Other authors on the study include first author Hiroki Nagai of Yale and the National Institute of Genetics; Jonathan C. Kagan of Yale; and Xinjun Zhu and Richard A. Kahn of Emory University School of Medicine

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Karen N. Peart: karen.peart@yale.edu, 203-980-2222