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Researcher from Rensselaer Polytechnic Institute (RPI) detected that bacterium Pseudomonas aeruginosa released molecules which make them able to prepare biofilm which in turn become more resistant against multiple antibiotics and these all things are urge by breakdown in respiratory chain and killing some of the population which trigger in formation of biofilm.
"What we've found is a suicidal pathway in which the sacrifice of some leads to a benefit for the community," said Blanca Barquera, an associate professor of biological sciences and member of the Center for Biotechnology and Interdisciplinary Studies (CBIS) at Rensselaer. "One of Pseudomonas' own molecules targets one of its own proteins, and while some die, the ones that survive are induced to make a biofilm. This research helps us to understand how Pseudomonas creates biofilms, and that could help us prevent biofilms that play a role in persistent and relapsing infections."
Pseudomonas is known to be an opportunistic pathogen and generally causes attacks on patient s having weakened immune system and involve in causing disease like Cystic fibrosis, Cancer, HIV and traumatic surgery. Researcher detected molecule named 2-n-heptyl-4-hydroxyquinoline-N-oxide (HQNQ) mainly used or communication by bacteria and Pseudomonas produces this molecules in high population densities.
"The survivors that are antibiotic tolerant cells make a biofilm," said Barquera. "We know that this is part of a signaling process, but how it is regulated is not yet clear and will require further research."
Note: The above story is for information purposes for more information go through original story sources.
Story source: Rensselaer Polytechnic Institute (RPI)
Journal References:
Ronen Hazan, Yok Ai Que, Damien Maura, Benjamin Strobel, Paul Anthony Majcherczyk, Laura Rose Hopper, David J. Wilbur, Teri N. Hreha, Blanca Barquera, Laurence G. Rahme. Auto Poisoning of the Respiratory Chain by a Quorum-Sensing-Regulated Molecule Favors Biofilm Formation and Antibiotic Tolerance. Current Biology, 2016; 26 (2): 195 DOI: 10.1016/j.cub.2015.11.056
