Severe infections (sepsis) are a common cause of admission to the intensive care unit. They represent a significant health risk for patients in the short and medium term. They are particularly linked to a change in the function of immune cells. In some patients, a state of pseudo-dormancy of monocyte and macrophage-type immune cells, called immunosuppression of myeloid cells, is observed. This situation leads to a worsening of the infection, so it should be avoided because it represents a danger for the patient even when they ar receiving antibiotics. At present, these events are still very poorly understood. Research is essential to understand how this state of immunosuppression of myeloid cells is established in order to adapt existing treatments or find new ones. Laboratory studies on animal models of septicaemia have shown that this state of immunosuppression of myeloid cells is closely linked to a change in the production of energy by myeloid cells (monocytes and macrophages). The functioning 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 septicaemia. The objective of this study is to verify whether alterations in mitochondrial function in myeloid cells also occur in patients with bacterial infection compared to patients without bacterial infection.
Study Type
OBSERVATIONAL
Enrollment
36
use of the remaining 1-2 ml of blood in samples taken as part of routine care to study mitochondrial function
Chu Dijon Bourgogne
Dijon, France
Level of mitophagy in circulating monocytes
Measurement of mitochondrial density and PINK1 protein expression by flow cytometry in circulating monocytes (total population and subpopulation of conventional, intermediate and non-conventional monocytes (CD33, CD16 and CD14 monocyte markers)
Time frame: <24 hours after hospitalization in intensive care
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