soluble NEUROPILIN-1 in sepsis correlates with organ dysfunction

Sepsis is a life-threatening medical condition that arises when the body’s response to an infection triggers widespread inflammation, leading to tissue damage and organ dysfunction. Early recognition and prompt treatment are crucial as sepsis can result in multi-organ failure and death (1). Timely administration of antibiotics and supportive care significantly improve outcomes, highlighting the importance of awareness and rapid intervention in managing this critical condition.

For sepsis, a range of biomarkers exist but have not been completely effective identifying patients at the onset of sepsis or in predicting their prognosis and the anticipated severity of organ failure. Furthermore, the mechanisms underlying the uncontrolled infection, dysregulated immune response, and subsequent organ failure remain unclear, highlighting the need for further research.

A recent study by Hohlstein P and colleagues (2) explores the role of soluble Neuropilin-1 (sNRP-1) in critical illness and sepsis and evaluates its potential as a biomarker in this context.

Key findings of the study:

• Critically ill and septic patients exhibit higher levels of circulating sNRP-1.
• sNRP-1 levels correlate with organ failure, particularly hepatic and kidney function impairment.
• Long-term survivors have lower levels of sNRP-1 upon admission to the ICU.

soluble NEUROPILIN-1 in sepsis correlates with organ dysfunction

Soluble Neuropilin-1 (sNRP-1) was measured in human serum samples with the

Biomedica soluble Neuropilin-1 ELISA assay (cat. no. BI-20409)

Assay Highlights:

• Only assay that detects free and ligand-bound soluble Neuropilin-1
• Highly specific and epitope mapped antibodies 
• Extensively validated according to FDA/ICH/EMEA guidelines

 

Links to the  Protocol Booklet and Validation Data

 

Soluble Neuropilin-1 Is Elevated in Sepsis and Correlates with Organ Dysfunction and Long-Term Mortality in Critical Illness. 

Abstract

Critical illness and sepsis may cause organ failure and are recognized as mortality drivers in hospitalized patients. Neuropilin-1 (NRP-1) is a multifaceted transmembrane protein involved in the primary immune response and is expressed in immune cells such as T and dendritic cells. The soluble form of NRP-1 (sNRP-1) acts as an antagonist to NRP-1 by scavenging its ligands. The aim of this study was to determine the value of sNRP-1 as a biomarker in critical illness and sepsis. We enrolled 180 critically ill patients admitted to a medical intensive care unit and measured serum sNRP-1 concentrations at admission, comparing them to 48 healthy individuals. Critically ill and septic patients showed higher levels of sNRP-1 compared to healthy controls (median of 2.47 vs. 1.70 nmol/L, p < 0.001). Moreover, sNRP-1 was also elevated in patients with sepsis compared to other critical illness (2.60 vs. 2.13 nmol/L, p = 0.01), irrespective of disease severity or organ failure. In critically ill patients, sNRP-1 is positively correlated with markers of kidney and hepatic dysfunction. Most notably, critically ill patients not surviving in the long term (one year after admission) showed higher concentrations of sNRP-1 at the time of ICU admission (p = 0.036), with this association being dependent on the presence of organ failure. Critically ill and septic patients exhibit higher serum concentrations of circulating sNRP-1, which correlates to organ failure, particularly hepatic and kidney dysfunction.

Keywords: Neuropilin-1; critical illness; human; immune system; inflammation; intensive care unit; mortality; prognosis; sepsis; survival

Literature

1. Sepsis and septic shock. Cecconi M, Evans L, Levy M, Rhodes A. Lancet. 2018 Jul 7;392(10141):75-87. doi: 10.1016/S0140-6736(18)30696-2. Epub 2018 Jun 21. PMID: 29937192.
2. Soluble Neuropilin-1 Is Elevated in Sepsis and Correlates with Organ Dysfunction and Long-Term Mortality in Critical Illness. Hohlstein P, Schumacher E, Abu Jhaisha S, Adams JK, Pollmanns MR, Schneider CV, Hamesch K, Horvathova K, Wirtz TH, Tacke F, Trautwein C, Weiskirchen R, Koch A. Int J Mol Sci. 2024 May 16;25(10):5438. doi: 10.3390/ijms25105438. PMID: 38791476.