Discovery Could Stop Toxic Bacteria

The chemical enzyme employed by the deadly Streptococci bacteria family to escape human immune system defenses has been isolated by UCSD researchers, providing new ways to prevent strep infections.

Flesh-eating pathogens and the bacteria that cause strep throat and toxic shock syndrome use the enzyme, which was discovered by a team led by Victor Nizet, an associate professor of pediatrics at UCSD and an infectious diseases physician at Children’s Hospital in San Diego.

Nizet and his colleagues studied the interaction between the bacteria and neutrophils, which are specialized white blood cells that help the body against infections. Previous research found that neutrophils release “nets,” composed of DNA and toxic compounds, that trap and kill some types of bacteria that have invaded the body, but UCSD researchers went a step further and isolated the enzyme that strep bacteria use to render the nets useless.

By evading the neutrophil nets, strep bacteria are able to spread throughout the body. However, Nizet and his team have found that disabling the gene that creates this enzyme makes strep bacteria vulnerable again, allowing the body to more quickly fight off infections.

Cancer, Normal Cells Get Chatty

Cancer and neighboring healthy cells have the ability to communicate with each other, which could offer insight into why cancer spreads to certain body organs but not others, according to the results of a new UCSD study.

The researchers used gene chip technology to show that two-way “conversations” take place between malignant and normal cells that allow the cancer cells to spread and form new tumors in distant organs. They also found that cancer cells can only move to new parts of the body if the native cells in that region “speak the same language” as the invading cancer cells.

Chief researcher David Tarin, a professor of pathology and member of UCSD’s Moores Cancer Center, and his team hope the findings will cause researchers to rethink the best way to attack cancer by providing future treatment to block the malignant cells’ target organ, rather than directly targeting the cancer cells themselves.