Novel inhibitory effect of galectin-3 on the respiratory burst induced by Staphylococcus aureus in human neutrophils
Artikel i vetenskaplig tidskrift, 2023

Among the responders to microbial invasion, neutrophils represent the earliest and perhaps the most important immune cells that contribute to host defense with the primary role to kill invading microbes using a plethora of stored anti-microbial molecules. One such process is the production of reactive oxygen species (ROS) by the neutrophil enzyme complex NADPH-oxidase, which can be assembled and active either extracellularly or intracellularly in phagosomes (during phagocytosis) and/or granules (in the absence of phagocytosis). One soluble factor modulating the interplay between immune cells and microbes is galectin-3 (gal-3), a carbohydrate-binding protein that regulates a wide variety of neutrophil functions. Gal-3 has been shown to potentiate neutrophil interaction with bacteria, including Staphylococcus aureus, and is also a potent activator of the neutrophil respiratory burst, inducing large amounts of granule-localized ROS in primed cells. Herein, the role of gal-3 in regulating S. aureus phagocytosis and S. aureus-induced intracellular ROS was analyzed by imaging flow cytometry and luminol-based chemiluminescence, respectively. Although gal-3 did not interfere with S. aureus phagocytosis per se, it potently inhibited phagocytosis-induced intracellular ROS production. Using the gal-3 inhibitor GB0139 (TD139) and carbohydrate recognition domain of gal-3 (gal-3C), we found that the gal-3-induced inhibitory effect on ROS production was dependent on the carbohydrate recognition domain of the lectin. In summary, this is the first report of an inhibitory role of gal-3 in regulating phagocytosis-induced ROS production.


reactive oxygen species

Staphylococcus aureus




Vignesh Venkatakrishnan

Göteborgs universitet

Chalmers, Life sciences, Kemisk biologi

Jonas Elmwall

Göteborgs universitet

Trisha Lahiri

Göteborgs universitet

Martina Sundqvist

Göteborgs universitet

Linda Bergqvist

Göteborgs universitet

Hakon Leffler

Lunds universitet

Ulf J. Nilsson

Lunds universitet

Amanda Welin

Linköpings universitet

Johan Bylund

Göteborgs universitet

Anna Karlsson-Bengtsson

Göteborgs universitet

Chalmers, Life sciences


0959-6658 (ISSN) 1460-2423 (eISSN)

Vol. 33 6 503-511

Glykosylering i humana neutrofiler vid sepsis och systemisk inflammation

Vetenskapsrådet (VR) (2018-03077), 2019-01-01 -- 2024-12-31.



Immunologi inom det medicinska området

Reumatologi och inflammation





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