AI Article Synopsis
- * Researchers used a transposon mutant library to identify bacterial factors affecting interleukin-8 responses in human airway cells, discovering that the proteases AprA and LasB degrade flagellin, a component that triggers immune recognition.
- * The findings suggest that these proteases work together as a backup system, helping P. aeruginosa to evade immune responses effectively.
Article Abstract
The opportunistic pathogen Pseudomonas aeruginosa is capable of establishing severe and persistent infections in various eukaryotic hosts. It encodes a wide array of virulence factors and employs several strategies to evade immune detection. In the present study, we screened the Harvard Medical School transposon mutant library of P. aeruginosa PA14 for bacterial factors that modulate interleukin-8 responses in A549 human airway epithelial cells. We found that in addition to the previously identified alkaline protease AprA, the elastase LasB is capable of degrading exogenous flagellin under calcium-replete conditions and prevents flagellin-mediated immune recognition. Our results indicate that the production of two proteases with anti-flagellin activity provides a failsafe mechanism for P. aeruginosa to ensure the maintenance of protease-dependent immune-modulating functions.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4693985 | PMC |
| http://dx.doi.org/10.1128/IAI.00939-15 | DOI Listing |
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