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Long, J., Zaborina, O., & Holbrook, C. (2008). Depletion of Intestinal Phosphate following Surgical Injury Activates the Virulence of P. aeruginosa causing Lethal Gut-Derived Sepsis. Surgery, 144(2), 189–197. Added by: Dr. Enrique Feoli (31/05/2025, 16:34) Last edited by: Dr. Enrique Feoli (31/05/2025, 16:35) |
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| Resource type: Journal Article DOI: 10.1016/j.surg.2008.03.045 ID no. (ISBN etc.): 0039-6060 BibTeX citation key: Long2008 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Heridas quirúrgicas Creators: Holbrook, Long, Zaborina Collection: Surgery |
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| Abstract |
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Background Here we explored the possibility that the opportunistic pathogen, Pseudomonas aeruginosa (P.a) senses low phosphate (Pi) as a signal of host injury and shifts to a lethal phenotype. Methods Virulence expression in P. aeruginosa was examined in vitro under low phosphate conditions by assessing expression of the PA-I lectin, a barrier dysregulating protein, pyocyanin and biofilm production, and PstS, a phosphate scavenging protein. Virulence expression in vivo was assessed using surgically injured mice (30\% hepatectomy) intestinally inoculated with P. aeruginosa (P.a). Results In vitro experiments demonstrated that acute phosphate depletion resulted in a significant (p=0.001) increase in the expression the PA-I lectin, biofilm, pyocyanin, and PstS. Surgical injury caused significant (p=.006) depletion of intestinal phosphate concentration and increased mortality (60\%) due to intestinal P.a which was completely prevented with oral phosphate supplementation and restoration of intestinal phosphate- neither of which were observed with systemic (IV) administration. PstS gene expression was 32-fold higher in P.a recovered from the cecum following hepatectomy indicating inadequate intestinal Pi. Conclusions Surgical injury- induced intestinal phosphate depletion shifts the phenotype of P. aeruginosa to express enhanced virulence in vitro and lethality in vivo. Intestinal phosphate repletion may be a novel strategy to contain pathogens associated with lethal gut-derived sepsis.
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