Related Experiment Video
Updated: May 12, 2026

Swine Model of Biofilm Infection and Invisible Wounds
Published on: June 16, 2023
Production of Pseudomonas aeruginosa Intercellular Small Signaling Molecules in Human Burn Wounds
Yok-Ai Que1, Ronen Hazan, Colleen M Ryan
1Department of Surgery, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02114, USA ; Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115, USA.
Abstract:
Pseudomonas aeruginosa has developed a complex cell-to-cell communication system that relies on low-molecular weight excreted molecules to control the production of its virulence factors. We previously characterized the transcriptional regulator MvfR, that controls a major network of acute virulence functions in P. aeruginosa through the control of its ligands, the 4-hydroxy-2-alkylquinolines (HAQs)-4-hydroxy-2-heptylquinoline (HHQ) and 3,4-dihydroxy-2-heptylquinoline (PQS). Though HHQ and PQS are produced in infected animals, their ratios differ from those in bacterial cultures. Because these molecules are critical for the potency of activation of acute virulence functions, here we investigated whether they are also produced during human P. aeruginosa acute wound infection and whether their ratio is similar to that observed in P. aeruginosa-infected mice. We found that a clinically relevant P. aeruginosa isolate produced detectable levels of HAQs with ratios of HHQ and PQS that were similar to those produced in burned and infected animals, and not resembling ratios in bacterial cultures. These molecules could be isolated from wound tissue as well as from drainage liquid. These results demonstrate for the first time that HAQs can be isolated and quantified from acute human wound infection sites and validate the relevance of previous studies conducted in mammalian models of infection.
Insights
Pseudomonas aeruginosa uses signaling molecules called HAQs in human wound infections, similar to mouse models. This confirms previous research and highlights their role in virulence.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Pseudomonas aeruginosa utilizes quorum sensing via signaling molecules to regulate virulence.
- The transcriptional regulator MvfR controls key virulence factors through ligands 4-hydroxy-2-alkylquinolines (HAQs), specifically 4-hydroxy-2-heptylquinoline (HHQ) and 3,4-dihydroxy-2-heptylquinoline (PQS).
- Observed differences in HHQ and PQS ratios between bacterial cultures and infected animal models suggest context-dependent production.
Observation:
- Investigated the presence and ratios of HHQ and PQS during human P. aeruginosa acute wound infections.
- Examined if these ratios mirror those found in P. aeruginosa-infected mice.
- Assessed if HAQs are detectable in human wound tissue and drainage.
Findings:
- Clinically relevant P. aeruginosa isolates produced detectable HAQs in human wound infections.
- The ratios of HHQ and PQS in human wounds were similar to those in infected animal models, not bacterial cultures.
- HAQs were successfully isolated and quantified from both human wound tissue and drainage fluid.
Implications:
- Demonstrates for the first time the isolation and quantification of HAQs from human acute wound infection sites.
- Validates the use of mammalian infection models for studying P. aeruginosa quorum sensing and virulence.
- Provides crucial insights into the in vivo role of HAQs in P. aeruginosa pathogenesis during human infections.
More Related Videos
Related Concept Videos
Gene Regulation in Microbial Communities: Quorum Sensing
Bacterial Signaling
Clinical Applications of Epidermal Stem Cells
Burn Injuries
The damage results in the death of skin cells, which can lead to a massive loss of fluid. Dehydration, electrolyte imbalance, and renal and circulatory failure follow, which can be fatal. Burn patients are treated with intravenous fluids to offset...
Phases of Wound Repair
Formation of Blood Clot
In case of deep injuries, trauma to blood vessels results in blood loss. In the meantime, phospholipids released from the ruptured endothelial cellular membrane are converted into arachidonic...

