About this trial
: Sepsis, now defined as life-threatening organ dysfunction due to a dysregulated host response to infection, is an important global health problem representing about a fifth of all global deaths. It can be associated, in some cases, with multiple organ failure and cytokine storm. The main objective of this study is to estimate and to compare the activation rate of the Nucleotide-binding domain Leucine Rich repeat containing Protein 3 (NLRP3) inflammasome in platelets between five groups of patients suffering from bacterial and/or viral sepsis, with different severity levels according to Sequential Organ Failure Assessment (SOFA) score to precise the platelets' implication in this cytokine storm.
Eligibility criteria
This trial accepts healthy volunteersQualifiers
For all groups: patients older than 18 years at inclusion and acceptation of participation by the patient, his relative or his legal representative (depending on the situation)
For groups 1, 2, 3 and 5: Patient with a confirmed sepsis (microbiological confirmation)
For group 4 : Patient non infected
Disqualifiers
Refusal of participation by the patient, his relative or his legal representative (depending on the situation)
Patients subject to a safeguard measure of justice
Patients younger than 18 years at inclusion
Trial population
Thirty patients will be included in each group: patients with leptospirosis, patients with bacterial infections including in-hospital-acquired-infections, patients with viral infection, patients non infected (control group). Fifty-one patients will be included in group of patients with viral infection SARS-COv2 +.
Trial design
Cohort
Cross-sectional
Treatments tested in this trial
Not listed
Trial groups
Trial outcomes
Primary outcomes
Nucleotide-binding domain Leucine Rich repeat containing Protein 3 activation
The primary outcome will be the evaluation of platelets' NLRP3 activation in septic patients according to the severity of the disease
Secondary outcomes
Confocal Microscopy
We aim to confirm the colocalization of NRLP3/ASC in inflammasome activation by confocal microscopy
Sponsors and contacts
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