Pseudomonas Aeruginosa Adhesion Mechanisms in Respiratory Infections

Pseudomonas aeruginosa is an opportunistic pathogen that poses a significant threat in respiratory infections, particularly in patients with compromised pulmonary defences such as those with cystic fibrosis or ventilator-associated pneumonia. The early stages of colonisation hinge on the bacterium’s ability to adhere to the mucosal surfaces of the airways, a process mediated by an array of cell-associated and secreted virulence factors. At the forefront are filamentous appendages such as type IV pili and flagella, which not only facilitate initial attachment but also generate mechanical forces that remodel the airway mucus, promoting microcolony formation. Concurrently, adhesive polysaccharides and outer membrane proteins stabilise these interactions and seed the production of extracellular polymeric substances that coalesce into biofilms. Such biofilms confer enhanced resistance to antibiotics and immune clearance. Host mucus and mucin glycoproteins play a dual role: they act as a physical barrier yet can be co-opted by P. aeruginosa to extract monosaccharides or serve as contractile substrates for pili, thereby influencing biofilm architecture. Understanding the molecular dialogue between bacterial adhesins and host mucosal components has led to insights into strategies for preventing colonisation, including targeting pilus retraction mechanisms, modulating mucin properties and designing adhesion-inhibiting agents.

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Pseudomonas Aeruginosa Adhesion Mechanisms in Respiratory Infections publication trend

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Technical terms

Biofilm: A structured community of bacterial cells embedded in a self-produced matrix of extracellular polymeric substances that adheres to surfaces.

Type IV pili: Thin, retractile filamentous structures on the bacterial surface that mediate initial attachment, twitching motility and mechanical interactions with mucus.

Twitching motility: A form of surface translocation powered by the extension and retraction of type IV pili, enabling cells to move across and colonise host tissues.

Mucins: Large, heavily glycosylated proteins that form the gel-like mucus barrier lining respiratory epithelia and interact with microbial adhesins.

Flagella: Whip-like appendages that rotate to propel bacteria and contribute to motility, adhesion and biofilm architecture.

References

1. Pseudomonas aeruginosa type IV pili actively induce mucus contraction to form biofilms in tissue-engineered human airways. PLOS Biology (2023).
2. Uncovering bacterial-mammalian cell interactions via single-cell tracking. BMC Biology (2024).
3. Mucins trigger dispersal of Pseudomonas aeruginosa biofilms. npj Biofilms and Microbiomes (2018).
4. Host Mucin Is Exploited by Pseudomonas aeruginosa To Provide Monosaccharides Required for a Successful Infection. mBio (2020).
5. A global genomic approach uncovers novel components for twitching motility-mediated biofilm expansion in Pseudomonas aeruginosa. Microbial Genomics (2018).