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Updated: Oct 8, 2026
Legionella pneumophila Outer Membrane Vesicles: Isolation and Analysis of Their Pro-inflammatory Potential on Macrophages
Published on: February 22, 2017
Ex vivo functional immune alterations in ICU patients with Legionnaires' Disease, a proof-of-concept study
Camille Allam1, William Mouton2, Chloé Albert-Vega2
1Hospices Civils de Lyon, Institut des Agents Infectieux, Centre National de Référence des Légionelles, Lyon, France; Université Lyon 1, INSERM, ENS de Lyon, CNRS, CIRI, UMR 5308, UMR S1111, Lyon, France.
Objectives:
Legionnaires' disease (LD), caused by Legionella pneumophila intracellular bacterium, leads to intensive care unit (ICU) admission in 20-40% of cases. While ICU-LD patients display lung injury or septic shock, their functional immune response remains poorly understood. This proof-of-concept study assessed ex vivo immune gene expression in ICU-LD and non-ICU-LD patients.
Methods:
Whole blood from ICU-LD (n=6), non-ICU-LD (n=8), LD-unrelated septic shock (n=14), and healthy volunteers (n=9) was stimulated with lipopolysaccharide (LPS). Expression of 93 immune-related genes was quantified using nCounter (NanoString Technologies) and expressed relative to healthy volunteers. Functional enrichment analyses were performed using the STRING database.
Results:
ICU-LD patients displayed a 1.6-fold higher number of less induced genes (35/93 vs 22/93) and lower gene expression (median log2(FC): -1.9 vs -1.2, p=0.0011) than non-ICU-LD. Top five pathways identified as enriched in ICU-LD but not in non-ICU-LD patients were cellular response to LPS, regulation of IFN-β production, I-κB/NF-κB complex, IFN regulatory factor complex, and TRAF6-mediated NF-κB activation.
Conclusions:
Ex vivo immune gene expression alterations were found in LD patients, particularly in ICU-LD patients. ICU-LD patients displayed lower expression of genes involved in crucial pathways for Legionella replication control. These preliminary findings support further studies to evaluate the impact of LD patients' immune response on disease severity.