Stephen M. Black (above) and a team of researchers have uncovered a new therapeutic target for treating acute lung injury.

Stephen M. Black and a team of researchers have uncovered information that could help with treatment for acute lung injury. A summary of their study recently appeared in The Journal of Biological Chemistry, where they noted that a bacterial infection can throw off the equilibrium of two key proteins in the lungs and also put patients at risk of a highly lethal acute lung injury (ALI).

As Stephen M. Black explained in a recent press release, “Bacteria can alter a single amino acid in the protein RhoA, pushing its activity level well above that of Rac1 and prompting blood vessels to leak and flood thousands of tiny air sacs in the lungs.” Fortunately there might be a biological shield that is able to protect RhoA from potentially lethal alterations.

Stephen M. Black compared activation of RhoA to a rapid-fire gun that does not require the operator to pause and reload. As he explained, “Activation of RhoA is an early, early event and it is a pathological activation. The cell cannot regulate it anymore. It just stays on.”

While RhoA was believed to be a cause of ALI, researchers had not previously known how it contributed to its development. Other causes of ALI include severe trauma that induces shock; common bacterial infections such as pneumonia; meconium aspiration; burns; and multiple transfusions. Researchers used human lung cells and mass spectrometry to learn that amino acid Y34 was altered in ALI. They then utilized 3-D computer modeling to map out how Y34 alteration affected RhoA functioning. They learned that this process turns RhoA into a steady-firing protein.

Stephen M. Black explains that patients can clear the bacterial infection with antibiotics and still die if they do not survive long enough for the body to go back to making normal RhoA. He and the other researchers will continue their research into Y34 as unanswered questions include how long RhoA can sustain the super-pace resulting from bacteria modification and whether non-bacterial causes of ALI will prompt the same RhoA alteration.

Learn more about this breakthrough in the official press release: http://news.gru.edu/archives/11676

You can also read more about Stephen M. Black and his research in this press release, or by viewing his bio on VisualCV: http://www.visualcv.com/StephenMBlack