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Related Experiment Video

Updated: Jun 30, 2025

The Creation of a Rat Model for Osteosarcopenia via Ovariectomy

The Creation of a Rat Model for Osteosarcopenia via Ovariectomy

Published on: February 21, 2025

Primary sarcopenia is associated with elevated spontaneous NET formation.

Irina Balazs^1,2, Manuel Stelzer¹, Julia Traub³

¹Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical University of Graz, Graz, Austria.

Frontiers in Cell and Developmental Biology

|March 20, 2024

Summary

Spontaneous neutrophil extracellular trap (NET) formation is elevated in sarcopenia patients, potentially contributing to inflammation. However, NET formation response to bacterial stimuli and neutrophil phagocytosis remain intact in sarcopenia, even with liver cirrhosis.

Keywords:

NET formation chronic inflammation cirrhosis neutrophils sarcopenia

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In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells

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Published on: June 12, 2017

Area of Science:

Immunology
Cell Biology
Gastroenterology

Background:

Sarcopenia, muscle loss, is a common complication of liver cirrhosis and can also occur independently.
Neutrophil function, including neutrophil extracellular trap (NET) formation, is implicated in chronic inflammation but understudied in sarcopenia.

Purpose of the Study:

To investigate alterations in neutrophil functions (phagocytosis, reactive oxygen species (ROS) production, NET formation) in patients with sarcopenia, with or without liver cirrhosis.

Main Methods:

Neutrophils were isolated from 92 patients (cirrhosis with sarcopenia, cirrhosis without sarcopenia, sarcopenia only) and 10 healthy controls.
Neutrophil functions were assessed via stimulation with E. coli, phorbol 12-myristate 13-acetate (PMA), or incubation medium.
NET formation was quantified using the DNA Area and NETosis Analysis (DANA) algorithm; phagocytosis and ROS production were measured using commercial kits.

Main Results:

Spontaneous NET formation was significantly higher in patients with sarcopenia alone compared to those with cirrhosis and sarcopenia, and healthy controls.
NET formation in response to PMA was decreased in all patient groups (cirrhosis, cirrhosis with sarcopenia, sarcopenia) compared to controls.
Neutrophil phagocytosis and ROS production showed no significant differences between patient groups and healthy controls.

Conclusions:

Elevated spontaneous NET formation in sarcopenia may contribute to chronic inflammation, but does not impair antibacterial defense mechanisms.
Neutrophil phagocytosis and ROS production are not significantly affected in sarcopenia patients.
The DANA algorithm is a viable tool for analyzing NET formation in clinical studies, suggesting potential for NET formation-based biomarkers in sarcopenia.