Purpose: The purpose of the present study was twofold: first, to assess the effect of prolonged intense exercise on total neutrophil elastase content in endurance-trained cyclists and to determine whether this is associated with postexercise falls in lipopolysaccharide (LPS)-stimulated neutrophil elastase release; and second, to determine the effect of carbohydrate (CHO) ingestion during exercise on these responses.
Methods: In a randomized design, nine trained male cyclists cycled for 2 h at 75% VO(2max) on two occasions with either CHO (6.4%, i.e., 64 g x L-1) or placebo (PLA) beverage ingestion before (5 mL x kg-1), during (2 mL x kg-1), and after (5 mL x kg-1) the exercise. Venous blood samples were obtained at rest, immediately postexercise, and at 1 h postexercise.
Results: After exercise, CHO ingestion was associated with a higher plasma glucose concentration (P < 0.05) and fewer numbers of circulating neutrophils compared with the PLA trial (P < 0.01). Neither exercise nor CHO ingestion affected total neutrophil elastase content, yet LPS-stimulated neutrophil elastase release fell postexercise by approximately 47% on the PLA trial (P < 0.01). Values did not change significantly from preexercise on the CHO trial.
Conclusions: These findings suggest that neither exercise nor CHO-beverage ingestion influences the total elastase content of neutrophils. Therefore, changes in neutrophil elastase content cannot account for the fall in LPS-stimulated neutrophil elastase release after prolonged intense exercise or for the blunting of this response with CHO ingestion.
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http://dx.doi.org/10.1249/01.MSS.0000078927.08049.A8 | DOI Listing |
Tuberc Respir Dis (Seoul)
January 2025
Division of Molecular and Clinical Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.
Background: Neutrophil elastase (NE) has been proposed as a potential biomarker for evaluating the severity and prognosis of bronchiectasis. This study aimed to compare bronchial lavage quantification of NE levels and activities with those of sputum.
Methods: A cross-sectional study was conducted in which 24 Vietnamese adults with bronchiectasis were enrolled from June 2023 to August 2023.
Int J Mol Sci
December 2024
School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China.
Neutrophil extracellular traps (NETs) formation is a key process in inflammatory diseases like gout, but the underlying molecular mechanisms remain incompletely understood. This study aimed to establish a model to examine the formation of NETs induced by monosodium urate (MSU) and phorbol 12-myristate 13-acetate (PMA) and to elucidate their molecular pathways. Laser confocal microscopy was used to visualize NET formation, while flow cytometry was employed to detect reactive oxygen species (ROS) production.
View Article and Find Full Text PDFNat Commun
January 2025
University/BHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
Corticosteroid binding globulin (CBG; SERPINA6) binds >85% of circulating glucocorticoids but its influence on their metabolic actions is unproven. Targeted proteolytic cleavage of CBG by neutrophil elastase (NE; ELANE) significantly reduces CBG binding affinity, potentially increasing 'free' glucocorticoid levels at sites of inflammation. NE is inhibited by alpha-1-antitrypsin (AAT; SERPINA1).
View Article and Find Full Text PDFAging Cell
January 2025
Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, USA.
Streptococcus pneumoniae (Sp; pneumococcus), the most common agent of community-acquired pneumonia, can spread systemically, particularly in the elderly, highlighting the need for adjunctive therapies. The airway epithelial barrier defends against bacteremia and is dependent upon apical junctional complex (AJC) proteins such as E-cadherin. After mouse lung challenge, pneumolysin (PLY), a key Sp virulence factor, stimulates epithelial secretion of an inflammatory eicosanoid, triggering the infiltration of polymorphonuclear leukocytes (PMNs) that secrete high levels of neutrophil elastase (NE), thus promoting epithelial damage and systemic infection.
View Article and Find Full Text PDFFEBS J
January 2025
Physics, Department of Molecular and Translational Medicine, University of Brescia, Italy.
Neutrophil elastase (NE) is released by activated neutrophils during an inflammatory response and exerts proteolytic activity on elastin and other extracellular matrix components. This protease is rapidly inhibited by the plasma serine protease inhibitor alpha-1-antitrypsin (AAT), and the importance of this protective activity on lung tissue is highlighted by the development of early onset emphysema in individuals with AAT deficiency. As a serpin, AAT presents a surface-exposed reactive centre loop (RCL) whose sequence mirrors the target protease specificity.
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