T regulatory cells activation and distribution are modified in critically ill patients with acute respiratory distress syndrome: A prospective single-centre observational study.


Journal

Anaesthesia, critical care & pain medicine
ISSN: 2352-5568
Titre abrégé: Anaesth Crit Care Pain Med
Pays: France
ID NLM: 101652401

Informations de publication

Date de publication:
02 2020
Historique:
received: 18 05 2019
revised: 18 07 2019
accepted: 20 07 2019
pubmed: 3 8 2019
medline: 13 1 2021
entrez: 3 8 2019
Statut: ppublish

Résumé

Acute respiratory distress syndrome (ARDS) is a common and fatal inflammatory condition. Whether T regulatory cells (Tregs) are beneficial or detrimental remains controversial, and longitudinal studies are lacking. Phenotyping of Tregs activation markers has been poorly reported. We aimed to evaluate quantitative and functional alterations in blood and bronchoalveolar Treg phenotype of ARDS patients. We performed a single-centre observational study in a French intensive care unit. The study enrolled 60 ARDS and 45 non-ARDS patients. Patients under 18years old or with immunosuppression (native or acquired) were excluded. Tregs phenotypes were assessed by flow cytometry, while cytokines were measured by multiplex-based assays in blood and bronchoalveolar samples collected over 3weeks after the onset of ARDS. Blood Tregs/CD4+ percentage (median %, 25-75% interquartile) was higher in ARDS patients than in non-ARDS patients: 12.1% [9.0-16.0] versus 9.9% [8.1-12.6], P=0.01. Alveolar Tregs/CD4+ percentage was lower in ARDS patients than in non-ARDS patients: 10.4% [6.3-16.6] versus 16.2% [12.4-21.1], P=0.03. In ARDS patients, Tregs activation was reduced in the blood and increased in the alveolus, compared to non-ARDS patients. ROC analysis revealed a threshold of 10.4% for the Tregs/CD4+ percentage in the blood collected within the first week of ARDS to discriminate between survivors and non-survivors (sensitivity: 75%; specificity 76%; area under the curve [95% confidence interval]: 0.72 [0.5-0.9]). Quantitative and functional alterations in Treg phenotype were observed in patients with ARDS. Whether rebalancing Tregs phenotype with therapeutic interventions would be beneficial deserves further investigations.

Sections du résumé

BACKGROUNDS
Acute respiratory distress syndrome (ARDS) is a common and fatal inflammatory condition. Whether T regulatory cells (Tregs) are beneficial or detrimental remains controversial, and longitudinal studies are lacking. Phenotyping of Tregs activation markers has been poorly reported. We aimed to evaluate quantitative and functional alterations in blood and bronchoalveolar Treg phenotype of ARDS patients.
METHODS
We performed a single-centre observational study in a French intensive care unit. The study enrolled 60 ARDS and 45 non-ARDS patients. Patients under 18years old or with immunosuppression (native or acquired) were excluded. Tregs phenotypes were assessed by flow cytometry, while cytokines were measured by multiplex-based assays in blood and bronchoalveolar samples collected over 3weeks after the onset of ARDS.
RESULTS
Blood Tregs/CD4+ percentage (median %, 25-75% interquartile) was higher in ARDS patients than in non-ARDS patients: 12.1% [9.0-16.0] versus 9.9% [8.1-12.6], P=0.01. Alveolar Tregs/CD4+ percentage was lower in ARDS patients than in non-ARDS patients: 10.4% [6.3-16.6] versus 16.2% [12.4-21.1], P=0.03. In ARDS patients, Tregs activation was reduced in the blood and increased in the alveolus, compared to non-ARDS patients. ROC analysis revealed a threshold of 10.4% for the Tregs/CD4+ percentage in the blood collected within the first week of ARDS to discriminate between survivors and non-survivors (sensitivity: 75%; specificity 76%; area under the curve [95% confidence interval]: 0.72 [0.5-0.9]).
CONCLUSIONS
Quantitative and functional alterations in Treg phenotype were observed in patients with ARDS. Whether rebalancing Tregs phenotype with therapeutic interventions would be beneficial deserves further investigations.

Identifiants

pubmed: 31374365
pii: S2352-5568(19)30210-3
doi: 10.1016/j.accpm.2019.07.014
pii:
doi:

Substances chimiques

Cytokines 0

Types de publication

Journal Article Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

35-44

Informations de copyright

Copyright © 2019 Société française d'anesthésie et de réanimation (Sfar). Published by Elsevier Masson SAS. All rights reserved.

Auteurs

Sebastien Halter (S)

Multidisciplinary Intensive Care Unit, Department of Anaesthesiology and Critical Care, La Pitié-Salpêtrière Hospital, Public Hospitals of Paris (AP-HP), Sorbonne University, 75013 Paris, France; Public Hospitals of Paris (AP-HP), La Pitié-Salpêtrière Hospital, Biotherapy (CIC-BTi) and Inflammation-Immunopathology-Biotherapy Department (i2B), 75651 Paris, France; Sorbonne University, INSERM, UMR_S 959, Immunology-Immunopathology-Immunotherapy (i3), 75651 Paris, France.

Lucrèce Aimade (L)

Public Hospitals of Paris (AP-HP), La Pitié-Salpêtrière Hospital, Biotherapy (CIC-BTi) and Inflammation-Immunopathology-Biotherapy Department (i2B), 75651 Paris, France; Sorbonne University, INSERM, UMR_S 959, Immunology-Immunopathology-Immunotherapy (i3), 75651 Paris, France.

Michèle Barbié (M)

Public Hospitals of Paris (AP-HP), La Pitié-Salpêtrière Hospital, Biotherapy (CIC-BTi) and Inflammation-Immunopathology-Biotherapy Department (i2B), 75651 Paris, France.

Hélène Brisson (H)

Multidisciplinary Intensive Care Unit, Department of Anaesthesiology and Critical Care, La Pitié-Salpêtrière Hospital, Public Hospitals of Paris (AP-HP), Sorbonne University, 75013 Paris, France.

Jean-Jacques Rouby (JJ)

Multidisciplinary Intensive Care Unit, Department of Anaesthesiology and Critical Care, La Pitié-Salpêtrière Hospital, Public Hospitals of Paris (AP-HP), Sorbonne University, 75013 Paris, France.

Olivier Langeron (O)

Multidisciplinary Intensive Care Unit, Department of Anaesthesiology and Critical Care, La Pitié-Salpêtrière Hospital, Public Hospitals of Paris (AP-HP), Sorbonne University, 75013 Paris, France.

David Klatzmann (D)

Public Hospitals of Paris (AP-HP), La Pitié-Salpêtrière Hospital, Biotherapy (CIC-BTi) and Inflammation-Immunopathology-Biotherapy Department (i2B), 75651 Paris, France; Sorbonne University, INSERM, UMR_S 959, Immunology-Immunopathology-Immunotherapy (i3), 75651 Paris, France.

Michelle Rosenzwajg (M)

Public Hospitals of Paris (AP-HP), La Pitié-Salpêtrière Hospital, Biotherapy (CIC-BTi) and Inflammation-Immunopathology-Biotherapy Department (i2B), 75651 Paris, France; Sorbonne University, INSERM, UMR_S 959, Immunology-Immunopathology-Immunotherapy (i3), 75651 Paris, France.

Antoine Monsel (A)

Multidisciplinary Intensive Care Unit, Department of Anaesthesiology and Critical Care, La Pitié-Salpêtrière Hospital, Public Hospitals of Paris (AP-HP), Sorbonne University, 75013 Paris, France; Public Hospitals of Paris (AP-HP), La Pitié-Salpêtrière Hospital, Biotherapy (CIC-BTi) and Inflammation-Immunopathology-Biotherapy Department (i2B), 75651 Paris, France; Sorbonne University, INSERM, UMR_S 959, Immunology-Immunopathology-Immunotherapy (i3), 75651 Paris, France. Electronic address: antoine.monsel@gmail.com.

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