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A Role for RAGE/TXNIP/Inflammasome Axis in Alveolar Macrophage Activation During ARDS (RIAMA): a Proof-of-concept Clinical Study

NCT02545621 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 20

Last updated 2020-05-12

No results posted yet for this study

Summary

RAGE (the receptor for advanced glycation end-products) is a marker of alveolar type I cell injury and a pivotal mediator of acute inflammation and innate immunity. RAGE pathway is highly regulated; the interaction of the transmembrane receptor with its various ligands (e.g. HMGB1, S100A12) ultimately leads to NF-kB activation and RAGE upregulation itself, but precise RAGE functions and intracellular pathways remain underexplored. During ARDS, monocyte and macrophage activation could modulate alveolar inflammation and repair.

As RAGE is also expressed at the surface of monocytes/macrophages, we hypothesize that alveolar monocyte/macrophage activation may be mediated through a RAGE-TXNIP (thioredoxin interacting protein)-NLRP3/inflammasome intracellular pathway. The purpose of this observational prospective study is to compare alveolar monocyte/macrophage activation profiles (as assessed by Fluorescence-Activated Cell Sorting (FACS)) in mechanically ventilated patients with or without ARDS.

Conditions

  • Acute Respiratory Distress Syndrome
  • Mechanical Ventilation

Interventions

OTHER

RAGE TXNIP Inflammasome axis

Sponsors & Collaborators

  • University Hospital, Clermont-Ferrand

    lead OTHER

Principal Investigators

  • Mathieu JABAUDON · University Hospital, Clermont-Ferrand

Eligibility

Min Age
18 Years
Max Age
95 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2015-09-30
Primary Completion
2016-09-30
Completion
2016-10-31

Countries

  • France

Study Locations

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT02545621 on ClinicalTrials.gov