Cardiogenic shock elicits acute inflammation, delayed eosinophilia, and depletion of immune cells in most severe cases.
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6 mai 2020
- doi: 10.1038/s41598-020-64702-0
- issn: 2045-2322
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info:eu-repo/semantics/altIdentifier/pmid/32377009
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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_855455087BEA1
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J. Cuinet et al., « Cardiogenic shock elicits acute inflammation, delayed eosinophilia, and depletion of immune cells in most severe cases. », Serveur académique Lausannois, ID : 10.1038/s41598-020-64702-0
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Patients with cardiogenic shock (CS) display systemic inflammation and a high rate of infections, suggesting important immune disturbances. To explore the immune response to CS, we prospectively measured, in 24 consecutive CS patients, differential white blood cell (WBC) counts and the cytokines IL-1β, IL-5, IL-6, IL-10, TNFα, IFNγ, MCP-1 and eotaxin (CCL11), at Day 1 (T1), day 3 (T2) and day 6-8 (T3). Secondary infections and their influence on cytokines and WBCs were determined. CS induced early (T1) neutrophilia and elevated levels of IL-6, IL-10 and MCP-1, correlating with shock severity. The eosinophil chemoattractant eotaxin was elevated at T1 and decreased thereafter, and a progressive rise of blood eosinophils was noted over time. Patients with the most severe shock had reduced lymphocytes and monocytes at T2 and T3. Sixty-two percent of patients developed an infection, which did not alter the profile of immune response, except from higher IL-6 levels at T2. Therefore, CS elicits an acute pro-inflammatory response, followed by a delayed increase in blood eosinophils, consistent with the development of a tissue repair response, as well as depletion of immune cells in the most severely affected patients, which might predispose to secondary infections.