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Cytotoxic rhamnolipid micelles drive acute virulence in . | LitMetric

AI Article Synopsis

  • The pathogen in question has developed resistance to many antibiotics, leading to increased infections and deaths, particularly among those with weakened immune systems.
  • The study highlights the role of rhamnolipid production in how this pathogen interacts with the host, showing that these substances are highly toxic to immune cells like macrophages.
  • The findings suggest that rhamnolipids contribute significantly to the pathogen's ability to cause harm and evade the immune response, emphasizing their role as critical virulence factors in infections.

Article Abstract

is an opportunistic human pathogen that has developed multi- or even pan-drug resistance towards most frontline and last resort antibiotics, leading to increasing infections and deaths among hospitalized patients, especially those with compromised immune systems. Further complicating treatment, produces numerous virulence factors that contribute to host tissue damage and immune evasion, promoting bacterial colonization and pathogenesis. In this study, we demonstrate the importance of rhamnolipid production in host-pathogen interactions. Secreted rhamnolipids form micelles that exhibited highly acute toxicity towards murine macrophages, rupturing the plasma membrane and causing organellar membrane damage within minutes of exposure. While rhamnolipid micelles (RMs) were particularly toxic to macrophages, they also caused membrane damage in human lung epithelial cells, red blood cells, Gram-positive bacteria, and even non-cellular models like giant plasma membrane vesicles. Most importantly, rhamnolipid production strongly correlated to virulence against murine macrophages in various panels of clinical isolates. Altogether, our findings suggest that rhamnolipid micelles are highly cytotoxic virulence factors that drive acute cellular damage and immune evasion during infections.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10592815PMC
http://dx.doi.org/10.1101/2023.10.13.562257DOI Listing

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