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ePaper created 2013-02-01, 09:35:07 | version 1.24.0
Research in Jülich 3|201214 How can new antibiotics knock out tuberculosis patho- gens? Dr. Lothar Eggeling from Forschungszentrum Jülich has the answer. His team and researchers from the University of Birmingham have isolated an enzyme of the tuberculosis bacteria that can be targeted by new drugs. T uberculosis was an epidemic until penicillin appeared on the market in the mid-1940s and banished “consumption” from Europe. Back then, even Alexander Fleming, who discovered this first antibiotic, warned that bacteria could easily become resistant to it. And he was right. According to the World Health Organization, the most important anti-tuberculosis drugs prove ineffective for every twentieth of the more than nine million new patients who contract tuberculosis worldwide every year. The need for new antibiotics is there- fore huge. In developing drugs to combat the bacteria that cause tuberculosis, re- searchers are focusing on finding their weak points. “We want to know where the bacteria’s metabolic pathways are particularly vulnerable, where their Achil- les’ heel is, so to speak,” says Dr. Lothar otics, they could see where the drugs were effective. The researchers found not one, but two targets: one of the anti- biotics docked onto a certain amino acid of DprE1, while another drug variant at- tached itself to a “loop” structure. Eggeling says, “The fact that we have identified not just one but two regions in DprE1 as potential targets for drugs sig- nificantly increases the chances of pro- ducing further variants of this group of new antibiotics and using them to devel- op new drugs.” :: Lothar Eggeling investigates the weak points of pathogens that allow antibiotics to attack them. Eggeling from the Institute of Bio- and Geosciences – Biotechnology. “However, we must understand the structure of the metabolic enzymes before we can target them with potential drugs.” Eggeling’s team successfully isolated a bacterial enzyme known as DprE1. A new group of antibiotic agents referred to as benzothiazinones bind to this en- zyme. The task of DPrE1 is to produce a building block for the bacterial cell wall. “This enzyme is absolutely vital for the bacteria,” emphasizes Eggeling. “That makes DprE1 a particularly suitable tar- get for attacks by antibiotics.” TWO WEAK POINTS The British colleagues discovered where these attacks take place. Using crystals made of the bacterial enzyme and different variants of the new antibi- The Achilles’ Heel of Tuberculosis Pathogens Tuberculosis patients in Davos – rest cures in the Swiss mountains were considered the only way of treating tuberculosis before penicillin was discovered.