Monocyte deactivation in neutropenic acute respiratory distress syndrome patients treated with granulocyte colony-stimulating factor

Details

Serval ID
serval:BIB_CE3C7B882575
Type
Article: article from journal or magazin.
Collection
Publications
Title
Monocyte deactivation in neutropenic acute respiratory distress syndrome patients treated with granulocyte colony-stimulating factor
Journal
Crit Care
Author(s)
Mokart D., Kipnis E., Guerre-Berthelot P., Vey N., Capo C., Sannini A., Brun J. P., Blache J. L., Mege J. L., Blaise D., Guery B. P.
ISSN
1466-609X (Electronic)
ISSN-L
1364-8535
Publication state
Published
Issued date
2008
Volume
12
Number
1
Pages
R17
Language
english
Notes
Mokart, Djamel
Kipnis, Eric
Guerre-Berthelot, Pierre
Vey, Norbert
Capo, Christian
Sannini, Antoine
Brun, Jean-Paul
Blache, Jean-Louis
Mege, Jean-Louis
Blaise, Didier
Guery, Benoit P
eng
Clinical Trial
England
Crit Care. 2008;12(1):R17. doi: 10.1186/cc6791. Epub 2008 Feb 18.
Abstract
INTRODUCTION: In severely neutropenic septic acute respiratory distress syndrome (ARDS) patients, macrophages and monocytes are the last potentially remaining innate immune cells. We have previously shown, however, a deactivation of the alveolar macrophage in neutropenic septic ARDS patients. In the present study, we tried to characterize in vitro monocyte baseline cytokine production and responsiveness to lipopolysaccharide exposure. METHODS: Twenty-two consecutive patients with cancer were prospectively enrolled into a prospective observational study in an intensive care unit. All patients developed septic ARDS and were divided into two groups: neutropenic patients (n = 12) and non-neutropenic patients (n = 10). All of the neutropenic patients received granulocyte colony-stimulating factor whereas no patient in the non-neutropenic group received granulocyte colony-stimulating factor. We compared monocytes from neutropenic patients with septic ARDS with monocytes from non-neutropenic patients and healthy control individuals (n = 10). Peripheral blood monocytes were cultured, and cytokine levels (TNFalpha, IL-1beta, IL-6, IL-10, and IL-1 receptor antagonist) were assayed with and without lipopolysaccharide stimulation. RESULTS: TNFalpha, IL-6, IL-10 and IL-1 receptor antagonist levels in unstimulated monocytes were lower in neutropenic patients compared with non-neutropenic patients. Values obtained in the healthy individuals were low as expected, comparable with neutropenic patients. In lipopolysaccharide-stimulated monocytes, both inflammatory and anti-inflammatory cytokine production were significantly lower in neutropenic patients compared with non-neutropenic patients and control individuals. CONCLUSION: Consistent with previous results concerning alveolar macrophage deactivation, we observed a systemic deactivation of monocytes in septic neutropenic ARDS. This deactivation participates in the overall immunodeficiency and could be linked to sepsis, chemotherapy and/or the use of granulocyte colony-stimulating factor.
Keywords
Adult, Cytokines/*biosynthesis, Female, Granulocyte Colony-Stimulating Factor/*therapeutic use, Humans, Lipopolysaccharides, Macrophage Activation, Male, Middle Aged, Monocytes/*metabolism, Neoplasms/complications, Neutropenia/complications/drug therapy/*metabolism/mortality, Respiratory Distress Syndrome/complications/*drug therapy/metabolism
Pubmed
Create date
29/04/2021 10:59
Last modification date
30/04/2021 6:38
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