Journal
NATURE COMMUNICATIONS
Volume 13, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41467-022-28967-5
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Funding
- National Institutes of Health (NIH) [RO1DK107713, R21AI110685-01, R01AI146349]
- Welch Foundation [I-2086]
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Pseudomonas aeruginosa secretes ExoT, a toxin that inhibits NLRC4-dependent inflammatory responses during wound infection. The T3SS recognition leads to phosphorylation cascade involving Abl/PKC delta/NLRC4, which activates NLRC4 inflammasome and initiates inflammatory responses to limit P. aeruginosa infection. ExoT functions as the main anti-inflammatory agent by targeting CrkII and blocking the phosphorylation cascade.
Pseudomonas aeruginosa secretes the toxin ExoT, which is important for pathogenesis. Here, the authors show that ExoT inhibits NLRC4-dependent inflammatory responses during wound infection. Type 3 Secretion System (T3SS) is a highly conserved virulence structure that plays an essential role in the pathogenesis of many Gram-negative pathogenic bacteria, including Pseudomonas aeruginosa. Exotoxin T (ExoT) is the only T3SS effector protein that is expressed in all T3SS-expressing P. aeruginosa strains. Here we show that T3SS recognition leads to a rapid phosphorylation cascade involving Abl / PKC delta / NLRC4, which results in NLRC4 inflammasome activation, culminating in inflammatory responses that limit P. aeruginosa infection in wounds. We further show that ExoT functions as the main anti-inflammatory agent for P. aeruginosa in that it blocks the phosphorylation cascade through Abl / PKC delta / NLRC4 by targeting CrkII, which we further demonstrate to be important for Abl transactivation and NLRC4 inflammasome activation in response to T3SS and P. aeruginosa infection.
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