Extract
Sepsis is a common cause of lung hyperinflammation and barrier failure, resulting in acute respiratory distress syndrome (ARDS). Despite antibiotics, mortality from bacterial sepsis increases in the developed world, suggesting injurious mechanisms beyond live bacteria. In addition to bacterial toxins, membrane vesicles (MVs) may present potential mechanisms of organ failure in sepsis. Bacterial MVs are extracellular vesicles formed from bacterial membranes [1] that can elicit systemic inflammatory responses, e.g. by inflammasome activation [2, 3]. Here, we tested whether MVs from a relevant sepsis pathogen, Pseudomonas aeruginosa, were sufficient to cause characteristic signs of acute lung injury (ALI), the preclinical analogue to ARDS, in vitro and in vivo.
Abstract
Membrane vesicles released by Pseudomonas aeruginosa PA14 can elicit septic acute lung injury due to loss of endothelial barrier integrity and inflammasome activation https://bit.ly/3gMnkPu
Acknowledgements
M.J. McVey is the recipient of a CIHR Vanier Scholarship.
Footnotes
Conflict of interest: M. Maishan has nothing to disclose.
Conflict of interest: A. Foley has nothing to disclose.
Conflict of interest: R. Turki has nothing to disclose.
Conflict of interest: E.J. Roach has nothing to disclose.
Conflict of interest: R. Deschler has nothing to disclose.
Conflict of interest: S. Weidenfeld has nothing to disclose.
Conflict of interest: N.M. Goldenberg has nothing to disclose.
Conflict of interest: C.M. Khursigara has nothing to disclose.
Conflict of interest: W.M. Kuebler has nothing to disclose.
Conflict of interest: M.J. McVey has nothing to disclose.
Support statement: W.M. Kuebler is supported by grants from the German Research Foundation (SFB-TR84 A2 and C9, SFB 1449 B1, SFB 1470 A4, KU1218/9-1, KU1218/11-1, and KU1218/12-1) and the German Ministry of Education and Research (BMBF) in the framework of SYMPATH (01ZX1906A) and PROVID (01KI20160A). C.M. Khursigara is supported by operating grants from the Canadian Institute of Health Research (CIHR; PJT 156111). N.M. Goldenberg is supported by CIHR and AstraZeneca Canada and Canadian Lung Association Early Career Scientist Awards as well as an International Anesthesia Research Society Mentored Research Award. M.J. McVey received financial support from Hospital for Sick Children Research Institute – Peter Gilgan Centre for Research and Learning start-up funds, a Canadian Hematology Society RK Smiley Research Grant and a Society of Pediatric Anesthesia Young Investigator Grant. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received May 26, 2021.
- Accepted February 4, 2022.
- Copyright ©The authors 2022. For reproduction rights and permissions contact permissions{at}ersnet.org
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