August 22 (HealthDay News) -- A molecule that tames bacteria that cause gastroenteritis, tularemia and severe diarrhea has been identified by researchers at the University of Texas Southwestern Medical Center at Dallas.

The finding, they say, could help in the development of new drugs to combat increasing microbial resistance to antibiotics.

The molecule LED209 blocks a bacterial receptor, called QseC sensor kinase, from biochemical signals from the host that trigger bacteria to release toxins and cause illness.

"What we have here is a completely novel approach to combating illness," study senior author Dr. Vanessa Sperandio, an associate professor of microbiology and biochemistry, said in a UT Southwestern news release.

In studies in vitro, the researchers found that LED209 blocked the QseC sensors in E. coli, salmonella, and Francisella tularensis bacteria. In mice, LED209 prevented salmonella and F. tularensis from causing illness.

The findings were published online Aug. 21 in Science.

Conventional antibiotics kill bacteria. Killing or inhibiting the growth of some bacteria "angers" them and causes them to release toxins. LED209 allows bacteria to grow but prevents virulence that causes illness, according to the study.

"The sensors in bacteria are waiting for the right signal to initiate expression of virulent genes," Sperandio explained. "Using LED209, we blocked those sensing mechanisms and basically tricked the bacteria to not recognize that they were within the host. When we did that, the bacterial pathogens could not effectively cause disease in the treated animals."

Allowing the bacteria to survive also reduces the likelihood it will develop drug resistance.

The study looked at how LED209 affected three pathogens, but the researchers believe that drugs that target QseC could have wider use, because the sensor is present in at least 25 important animal and plant pathogens, including those that cause lung infections and Legionnaire's disease.

SOURCE: University of Texas Southwestern Medical Center at Dallas, news release, Aug. 21, 2008