Immune Profiling Demonstrates a Common Immune Signature of Delayed Acquired Immunodeficiency in Patients With Various Etiologies of Severe Injury
- PMID: 34534131
- DOI: 10.1097/CCM.0000000000005270
Immune Profiling Demonstrates a Common Immune Signature of Delayed Acquired Immunodeficiency in Patients With Various Etiologies of Severe Injury
Erratum in
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Immune Profiling Demonstrates a Common Immune Signature of Delayed Acquired Immunodeficiency in Patients With Various Etiologies of Severe Injury: Erratum.Crit Care Med. 2022 Jun 1;50(6):e618. doi: 10.1097/CCM.0000000000005565. Epub 2022 May 19. Crit Care Med. 2022. PMID: 35617575 No abstract available.
Abstract
Objectives: The host response plays a central role in the pathophysiology of sepsis and severe injuries. So far, no study has comprehensively described the overtime changes of the injury-induced immune profile in a large cohort of critically ill patients with different etiologies.
Design: Prospective observational cohort study.
Setting: Adult ICU in a University Hospital in Lyon, France.
Patients: Three hundred fifty-three septic, trauma, and surgical patients and 175 healthy volunteers were included in the REAnimation Low Immune Status Marker study.
Interventions: None.
Measurements and main results: Extensive immune profiling was performed by assessing cellular phenotypes and functions, protein, and messenger RNA levels at days 1-2, 3-4, and 5-7 after inclusion using a panel of 30 standardized immune markers. Using this immunomonitoring panel, no specificity in the immune profile was observed among septic, trauma, and surgical patients. This common injury-induced immune response was characterized by an initial adaptive (i.e., physiologic) response engaging all constituents of the immune system (pro- and anti-inflammatory cytokine releases, and innate and adaptive immune responses) but not associated with increased risk of secondary infections. In contrary, the persistence in a subgroup of patients of profound immune alterations at the end of the first week after admission was associated with increased risk of secondary infections independently of exposure to invasive devices. The combined monitoring of markers of pro-/anti-inflammatory, innate, and adaptive immune responses allowed a better enrichment of patients with risk of secondary infections in the selected population.
Conclusions: Using REAnimation Low Immune Status Marker immunomonitoring panel, we detected delayed injury-acquired immunodeficiency in a subgroup of severely injured patients independently of primary disease. Critically ill patients' immune status could be captured through the combined monitoring of a common panel of complementary markers of pro-/anti-inflammatory, innate, and adaptive immune responses. Such immune monitoring needs to be incorporated in larger study cohorts with more extensive immune surveillance to develop specific hypothesis allowing for identification of biological systems affecting altered immune function related to late infection in the setting of acute systemic injury.
Trial registration: ClinicalTrials.gov NCT02638779.
Copyright © 2021 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
Conflict of interest statement
Drs. Textoris, Blein, Moucadel, and Pachot are employees of bioMérieux SA, an in vitro diagnostic company. Drs. Venet, Bouffard, Delwarde, Martin, Girardot, Truc, Monneret, and Rimmelé are employees of Hospices Civils de Lyon. Drs. Venet, Textoris, Blein, Moucadel, Pachot, Monneret, and Rimmelé work in a joint research unit, cofunded by the Hospices Civils de Lyon and bioMérieux. Drs. Venet, Textoris, Pachot, and Monneret are coinventors in patent applications covering the following markers: CX3CR1, CD127, interleukin-10, and S100A9. Drs. Tan and Tipple are employees of and hold stock and shares in GlaxoSmithKline. Dr. Cortez is an employee of Sanofi Pasteur. Dr. Cortez was an employee of Sanofi. Drs. Venet’s, Textoris’s, Blein’s, Rol’s, Canard’s, Tipple’s, Vedrine’s, Martin’s, Girardot’s, Truc’s, Griffiths’s, Pachot’s, and Rimmelé’s institutions received funding from the Agence Nationale de la Recherche through a grant awarded to BIOASTER (ANR-10-AIRT-03), bioMerieux, Sanofi, and GSK. Dr. Bodinier received funding from HCL. Drs. Quemeneur and Moucadel disclosed work for hire. Dr. Quemeneur disclosed that his partner is an employee of Bioaster. Dr. Martin disclosed government work. The remaining authors have disclosed that they do not have any potential conflicts of interest.
Comment in
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Inflamed.Crit Care Med. 2022 Apr 1;50(4):691-693. doi: 10.1097/CCM.0000000000005293. Crit Care Med. 2022. PMID: 35311777 No abstract available.
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