Bacterial Protein Impairs Important Cellular Processes

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Pseudomonas aeruginosa is a widespread and problematic bacterium that can cause disease in plants and humans, especially where there is an existing disease or injury. Because the Pseudomonas aeruginosa bacterium is particularly resistant to antibiotics, the World Health Organization (WHO) categorizes it as "Priority 1/CRITICAL" on the global list of priority pathogens.

Recently, Dr. Winfried Römer of the University of Freiburg found that Pseudomonas aeruginosa lectins (proteins that bind to carbohydrates), specifically LecB, can block the normal cell cycle of bacterium host cells—meaning wounds heal slower, or not at all.

Römer and her team found that when LecB is present in infected wounds, it’s possible for Pseudomonas aeruginosa to remain and persist. Additionally, LecB can cause the interior of the infected cell to degrade by means of the degradation of growth factor receptors. In a normal cell, growth factors bind to growth factor receptors, which accelerates tissue growth. Alessa Landi, a member of Römer’s research team and the first author of the paper published in Life Science Alliance, said, “We were surprised that LecB does not contribute to the activation of growth factor signaling pathways, but that it triggers this silent internalization of receptors without activation.”

Römer’s research team also discovered how LecB blocks the cell cycle. First, there is a development of larger, enclosed vacuoles within the host cell. LecB enriches the plasma membranes that help to form these vacuoles, which interferes with the cell cycle.

“Although lectins are not catalytically active, LecB appears to interfere with important host cell processes, like the cell cycle, in a way we don't yet understand,” explained Römer.

Based on their findings so far, Römer’s and her team will be conducting further research about Aeruginosa lectin LecB. Römer believes that LecB may also facilitate the spread of bacteria in immune cells, so the next step is to examine how LecB compromises the immune response in humans with chronic wound infections.

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