Increased Alveolar Epithelial Damage Markers and Inflammasome-Regulated Cytokines Are Associated with Pulmonary Superinfection in ARDS

Author:

Peukert Konrad1,Sauer Andrea1,Seeliger Benjamin2ORCID,Feuerborn Caroline1,Fox Mario1,Schulz Susanne1,Wild Lennart1,Borger Valeri3ORCID,Schuss Patrick34ORCID,Schneider Matthias3ORCID,Güresir Erdem35,Coburn Mark1,Putensen Christian1,Wilhelm Christoph6,Bode Christian1ORCID

Affiliation:

1. Department of Anesthesiology and Intensive Care Medicine, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany

2. Department of Respiratory Medicine and German Centre of Lung Research (DZL), Hannover Medical School, Carl-Neuberg-Str. 1, 30635 Hannover, Germany

3. Department of Neurosurgery, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany

4. Department of Neurosurgery, BG Klinikum Unfallkrankenhaus Berlin gGmbH, Warener Str. 7, 12683 Berlin, Germany

5. Department of Neurosurgery, University Hospital Leipzig, Liebig Str. 20, Haus 4, 04103 Leipzig, Germany

6. Institute of Clinical Chemistry and Clinical Pharmacology, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany

Abstract

Acute respiratory distress syndrome (ARDS) is a life-threatening form of respiratory failure defined by dysregulated immune homeostasis and alveolar epithelial and endothelial damage. Up to 40% of ARDS patients develop pulmonary superinfections, contributing to poor prognosis and increasing mortality. Understanding what renders ARDS patients highly susceptible to pulmonary superinfections is therefore essential. We hypothesized that ARDS patients who develop pulmonary superinfections display a distinct pulmonary injury and pro-inflammatory response pattern. Serum and BALF samples from 52 patients were collected simultaneously within 24 h of ARDS onset. The incidence of pulmonary superinfections was determined retrospectively, and the patients were classified accordingly. Serum concentrations of the epithelial markers soluble receptor for advanced glycation end-products (sRAGE) and surfactant protein D (SP-D) and the endothelial markers vascular endothelial growth factor (VEGF) and angiopoetin-2 (Ang-2) as well as bronchoalveolar lavage fluid concentrations of the pro-inflammatory cytokines interleukin 1ß (IL-1ß), interleukin 18 (IL-18), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-a) were analyzed via multiplex immunoassay. Inflammasome-regulated cytokine IL-18 and the epithelial damage markers SP-D and sRAGE were significantly increased in ARDS patients who developed pulmonary superinfections. In contrast, endothelial markers and inflammasome-independent cytokines did not differ between the groups. The current findings reveal a distinct biomarker pattern that indicates inflammasome activation and alveolar epithelial injury. This pattern may potentially be used in future studies to identify high-risk patients, enabling targeted preventive strategies and personalized treatment approaches.

Publisher

MDPI AG

Subject

General Medicine

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