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Scientists at the Binghamton University, State University of New York claim to have buttoned down three essential regulators that were needed for the formation and development of biofilms. Apparently this discovery could pave new ways for treating chronic infections.

Biofilms are believed to be communities of bacteria in self-produced slime that could be found almost anywhere solids and liquids meet like in nature, in hospitals or in industrial settings. As per the Centers for Disease Control, biofilms are known to have been implicated in over 80 percent of chronic inflammatory and infectious diseases which may be caused by bacteria. This supposedly comprises of ear infections, gastrointestinal ulcers, urinary tract infections and pulmonary infections in cystic fibrosis patients.

According to the researchers, biofilms may be tough to destroy through traditional antimicrobial treatments as they can be nearly 1,500-fold more resistant to antibiotics as compared to planktonic, free-floating cells. Besides, biofilms also seem to pose a persistent problem in many industrial processes like drinking water distribution networks and manufacturing.

The important regulatory events needed for the formation and development of Pseudomonas aeruginosa biofilms was put forth by Karin Sauer, associate professor of biology at Binghamton University, and graduate student Olga Petrova.

“We have found a pathway of how the formation of biofilms is controlled,” Sauer mentioned. “If we can figure out how to make use of this newly discovered genetic program, we can interfere with the formation of biofilms and either prevent or treat biofilm infections more successfully.”

Supposedly Pseudomonas aeruginosa is an opportunistic pathogenic bacterium. It is considered to be one of the primary causes of death in patients who suffer from cystic fibrosis. An earlier unknown genetic program that composed of many regulators was documented by Petrova. This was apparently done by searching for alterations in the patterns of phosphorylation in Pseudomonas aeruginosa. It was observed that these regulators could not only be used to prevent the development of biofilms at various stages in their growth but also to revert established biofilms to a previous developmental stage.

“The problem you have when you have a chronic infection is that your immune system is trying to clear the infection but is unable to,” Sauer further commented. “And the longer the chronic infection goes on, the more damage there will be to tissue at the site of the infection. That’s because the immune response often involves the release of toxic compounds that have no effect on biofilms but can damage the surrounding tissues.”

Sauer’s research claims to be driven by several key questions like ‘Can we outsmart the biofilms? Can we interfere with biofilm antibiotic resistance? Can we figure out how to prevent biofilms from forming and becoming resistant to antibiotics?’

Apparently, some latest findings seem to answer these questions with a resounding yes. Besides needing regulators for biofilm formation, Sauer and her team had also recently recognized a regulator that could only be expressed in biofilms. It appears to be responsible for regulating antibiotic resistance.

This research is published in PLoS Pathogens, a peer-reviewed, open-access journal published online by the Public Library of Science.