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.