Taiwanese researchers have unlocked a key mechanism of a so-called “superbug” in a breakthrough that could lead to improved vaccines and treatment strategies to counter the pathogen.
National Sun Yat-sen University associate professor of marine biotechnology Lee I-ming (李益銘) and Academia Sinica Institute of Biological Chemistry adjunct research fellow Wu Shih-hsiung (吳世雄) headed the team that cracked a crucial molecule in Acinetobacter baumannii, the university said in a news release on Thursday.
The highly drug-resistant germ has a mortality rate of between 30 percent and 70 percent in patients and is listed by the WHO as a “top priority pathogen” that urgently requires new treatment options, the university said.
Photo: Hsu Li-chuan, Taipei Times
The bacterium has an exopolysaccharide coating that acts as a form of armor, protecting the germ from antibiotics and detection by the human immune system, while triggering severe inflammatory responses that could lead to pneumonia or sepsis, it said.
Using a phage, a virus that targets bacteria, the team cracked the germ’s shell to find fragments composed of O-acetylated pentasaccharide, the “chemical switch” that causes inflammation, the university said.
The acetylation marks are catalysts that activate the toll-like receptor 4 in immune cells, which governs inflammation, it said.
The research has significant implications, as finding a method to eliminate the markers would counter harmful inflammatory responses, it said.
The discovery could be utilized to develop vaccines that target specific acetylation sites instead of the whole exopolysaccharide coating, allowing jabs with superior therapeutic effectiveness and fewer side-effects than conventional designs, the news release cited Lee as saying.
The research team also proposes an alternative medical strategy of using phage-derived enzymes to pry gaps in the bacterium’s exopolysaccharide armor, rendering the pathogen vulnerable to drugs and natural immune responses, the university said.
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