Deactivation of alveolar macrophages in septic neutropenic ARDS

Détails

ID Serval
serval:BIB_527C725A87D5
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Deactivation of alveolar macrophages in septic neutropenic ARDS
Périodique
Chest
Auteur⸱e⸱s
Mokart D., Guery B. P., Bouabdallah R., Martin C., Blache J. L., Arnoulet C., Mege J. L.
ISSN
0012-3692 (Print)
ISSN-L
0012-3692
Statut éditorial
Publié
Date de publication
08/2003
Volume
124
Numéro
2
Pages
644-52
Langue
anglais
Notes
Mokart, Djamel
Guery, Benoit P
Bouabdallah, Reda
Martin, Claude
Blache, Jean-Louis
Arnoulet, Christine
Mege, Jean-Louis
eng
Chest. 2003 Aug;124(2):644-52. doi: 10.1378/chest.124.2.644.
Résumé
STUDY OBJECTIVES: Neutrophils often have been involved in the pathophysiology of ARDS. However, authentic ARDS has been described in patients with severe neutropenia, suggesting the presence of other potential mechanisms that are responsible of this syndrome. Alveolar macrophages (AMs) could be involved in the development of ARDS, and so we decided to study AM activation in neutropenic patients. PATIENTS: We designed a prospective study and enrolled two subgroups of consecutive patients (group A, 18 patients; group B, 22 patients) with septic ARDS. In the first period, 7 of 18 patients were neutropenic, and in the second period 10 of 22 patients were neutropenic. All neutropenic patients were treated with granulocyte colony-stimulating factor (G-CSF). MEASUREMENTS AND RESULTS: In group A, BAL fluid samples were analyzed for differential and total cell counts, and alveolar activation marker expression (ie, human leukocyte antigen [HLA]-DR locus) was determined. Basal and lipopolysaccharide (LPS)-stimulated production of tumor necrosis factor, interleukin (IL)-1 beta, IL-6, and IL-10 was evaluated in group B. In neutropenic patients, the BAL fluid total cell count and the neutrophil absolute count was significantly lower compared to those in nonneutropenic patients (p = 0.029 and p = 0.046, respectively). HLA-DR expression on AMs was significantly decreased (p = 0.016), and the percentage of AMs expressing HLA-DR was also significantly lower (p = 0.041). In neutropenic patients, the mean percentage of AMs expressing HLA-DR was significantly lower in deceased patients compared to survivors (30 +/- 7 vs 43 +/- 1, respectively; p = 0.047). Basal AMs released cytokines was comparable between the two groups; however, LPS stimulation yielded a deactivation of AMs in neutropenic patients. CONCLUSION: These results suggest a deactivation and/or hypoactivation of AMs in septic ARDS patients. This deactivation/hypoactivation could be linked to the use of G-CSF as this molecule has been shown to generate a down-regulation of HLA-DR expression.
Mots-clé
Adult, Aged, Cytokines/biosynthesis, Female, Granulocyte Colony-Stimulating Factor/therapeutic use, HLA-DR Antigens/*metabolism, Humans, Macrophage Activation, Macrophages, Alveolar/*metabolism, Male, Middle Aged, *Neutropenia/complications/drug therapy/mortality, Prognosis, Prospective Studies, *Respiratory Distress Syndrome/complications/mortality/physiopathology
Pubmed
Création de la notice
29/04/2021 10:59
Dernière modification de la notice
30/04/2021 6:38
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