期刊
SURGERY
卷 144, 期 2, 页码 189-197出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.surg.2008.03.045
关键词
-
类别
资金
- NIGMS NIH HHS [R01 GM062344-08, R01-GM62344-06, R01 GM062344] Funding Source: Medline
Background. We explored the possibility that the opportunistic pathogen, Pseudomonas aeruginosa 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 PSIS, a phosphate scavenging protein. Virulence expression in vivo was assessed using operatively injured mice (30% hepatectomy) intestinally inoculated with P aeruginosa. Results. In vitro experiments demonstrated that acute phosphate depletion resulted in an increase (P = .001) in the expression the PA-I lectin, biofilm, pyocyanin, and PstS. Operative injury caused a depletion (P = .006) of intestinal phosphate concentration and increased mortality (60%) owing to intestinal P aeruginosa, which was prevented completely 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 aeruginosa recovered from the cecum after hepatectomy indicating inadequate intestinal Pi. Conclusions. Operative 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据