The role of the sensor kinase, QseC, an adrenergic receptor of Escherichia coli, in bacterial translocation during hemorrhagic shock.
Meng Jun,Huang Yun-Chao,Huang Jie,Yang Kun
The journal of trauma and acute care surgery
BACKGROUND:Hemorrhagic shock results in ileal mucosa damage and intestinal bacterial translocation. Additionally, during hemorrhagic shock, norepinephrine levels increase. Past research has shown that the QseC sensor kinase of Escherichia coli modulates the quorum-sensing response to epinephrine and norepinephrine. Therefore, the aim of our study was to examine whether the absence of the ability of E. coli to sense epinephrine/norepinephrine would attenuate the bacterial translocation to extraintestinal organs in a rat model of hemorrhagic shock. METHODS:An E. coli MC1000 qseC mutant was constructed, and E. coli MC1000 and MC1000ΔqseC with streptomycin resistance were used to track bacterial translocation after gavage in rats. A rat model of nonlethal hemorrhagic shock was used. The rats were divided into six groups: controls (SS), rats that received a sham shock and MC1000 (M-SS), rats that received a sham shock and MC1000ΔqseC (Δ-SS), rats that received a hemorrhagic shock alone (HS), rats that received a hemorrhagic shock and MC1000 (M-HS), and rats that received a hemorrhagic shock and MC1000ΔqseC (Δ-HS). RESULTS:We found the incidence of bacterial translocation in the M-HS rats was higher than in the Δ-HS rats. The observed effects seem to be largely dependent on the inability to sense epinephrine/norepinephrine and the decreased motility of E. coli MC1000ΔqseC. CONCLUSION:Therefore, a role for E. coli sensing epinephrine/norepinephrine in the pathophysiology of bacterial translocation following hemorrhagic shock is proposed. The demonstration of such an effect would suggest a new mechanism for the development of shock-induced sepsis.
The Epinephrine/Norepinephrine/Autoinducer-3 Interkingdom Signaling System in Escherichia coli O157:H7.
Moreira Cristiano G,Sperandio Vanessa
Advances in experimental medicine and biology
Epinephrine/norepinephrine/AI-3 signaling is used as an interkingdom chemical signaling system between microbes and their hosts. This system is also exploited by pathogens to regulate virulence traits. In enterohemorrhagic E. coli (EHEC) O157:H7, it is essential for pathogenesis and flagella motility. These three signals activate expression of a pathogenicity island named locus of enterocyte effacement (LEE), Shiga toxin, and the flagella regulon. These signals are sensed by the two-component system QseBC, whereas the bacterial membrane receptor QseC autophosphorylates and phosphorylates the QseB response regulator initiating a complex phosphorelay signaling cascade that activates the expression of a second two-component system, QseEF. The QseEF two-component system is also involved in the expression of the virulence genes, and it senses epinephrine, phosphate, and sulfate. This complex signaling cascade still needs to be completely elucidated.