Severe infections (sepsis) are a frequent cause of admission to the intensive care unit. Sepsis represent a significant risk for the health of patients in the short and medium term. Sepsis are notably linked to a change in the function of immune cells. In some patients, a state of pseudo-dormancy of monocyte and macrophage immune cells, called myeloid cell immunosuppression, is observed. This situation, which leads to a worsening of the infection, must be avoided because it represents a danger for the patient, even during antibiotic therapy. At present, these events are still very poorly understood. Research is needed to understand how the immunosuppression of myeloid cells occurs in order to adapt existing treatments or to find new ones. Laboratory work on animal models of sepsis has shown that this state of myeloid cell immunosuppression is closely linked to a modification of energy production by myeloid cells (monocytes and macrophages). The function of the mitochondria ("energy factory" of the cells) in these cells is impaired. Thus, restoring mitochondrial function in myeloid cells could be a therapeutic solution against the immunosuppression of myeloid cells during severe sepsis. The aim of this study is to verify whether alterations in mitochondrial function in myeloid cells occur in both patients with and without bacterial infection.
Study Type
INTERVENTIONAL
Allocation
NON_RANDOMIZED
Purpose
OTHER
Masking
NONE
Enrollment
205
Sampling of 2 tubes of 3 ml: * patient: H0: 0-6h post-admission * healthy volunteer: at inclusion
Collection of 2 tubes of 3 ml (H24: 24-30h post-admission)
clinical and biological medical data for patients and general health data for healthy volunteers
Chu Dijon Bourgogne
Dijon, France
Level of mitophagy
Time frame: at admission and at 24 hours post-admission
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