Deactivation of alveolar macrophages in septic neutropenic ARDS

Details

Serval ID
serval:BIB_527C725A87D5
Type
Article: article from journal or magazin.
Collection
Publications
Title
Deactivation of alveolar macrophages in septic neutropenic ARDS
Journal
Chest
Author(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
Publication state
Published
Issued date
08/2003
Volume
124
Number
2
Pages
644-52
Language
english
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.
Abstract
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.
Keywords
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
Create date
29/04/2021 9:59
Last modification date
30/04/2021 5:38
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