Abstract
SUMMARYHearing loss is frequent in intensive care patients and can be due to several causes. However, sepsis has not been examined as a possible cause. The aim of this study is to assess the influence of experimental sepsis on hearing thresholds and to evaluate pathological changes in the cochlea. The cecal ligation puncture technique was used to induce sepsis in 18 mice. Results were compared with those from 13 sham-operated and 13 untreated control mice. The hearing thresholds of the animals were evaluated with auditory evoked brainstem responses prior to the induction of sepsis and again at the peak of the disease. Immediately after the second measurement, the mice were sacrificed and the inner ears harvested and prepared for further evaluation. The cochleae were examined with light microscopy, electron microscopy and immunohistochemistry for Bax, cleaved caspase-3 and Bcl-2. The mice with sepsis showed a significant hearing loss but not the control groups. Induction of apoptosis could be shown in the supporting cells of the organ of Corti. Furthermore, excitotoxicity could be shown at the basal pole of the inner hair cells. In this murine model, sepsis leads to significant hearing impairment. The physiological alteration could be linked to apoptosis in the supporting cells of the organ of Corti and to a disturbance of the synapses of the inner hair cells.
Highlights
The incidence of sepsis is still high, with up to three cases per 1000 population per year, more than half of them requiring intensive care management (Angus et al, 2001)
Our group demonstrated the involvement of the inner ear in murine cerebral malaria, a systemic inflammatory disease (Schmutzhard et al, 2010) showing apoptosis in the fibrocytes of the spiral ligament, which play an essential role in the electrolyte circulation of the cochlea, and a breakdown of the blood-labyrinth
Hearing animals were infected using the cecal ligation puncture technique, and the hearing of the mice was assessed at the peak of the disease
Summary
The incidence of sepsis is still high, with up to three cases per 1000 population per year, more than half of them requiring intensive care management (Angus et al, 2001). Multi-organ failure includes involvement of the central nervous system, peripheral nerves and skeletal muscles (Latronico and Bolton, 2011), but so far systemic sepsis has not been linked to hearing impairment. Hearing loss has been accepted as an unappreciated phenomenon in critical care. Our group demonstrated the involvement of the inner ear in murine cerebral malaria, a systemic inflammatory disease (Schmutzhard et al, 2010) showing apoptosis in the fibrocytes of the spiral ligament, which play an essential role in the electrolyte circulation of the cochlea, and a breakdown of the blood-labyrinth. The fact that no malaria-typical alterations, like microhemorrhages or leukocyte sequestration, could be found in the temporal bones suggests that the pathological findings in the inner ear might be linked to the systemic inflammatory reaction
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