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Galectin-3 is a target for proteases involved in the virulence of Staphylococcus aureus.

Journal article
Authors Jonas Elmwall
Jakub Kwiecinski
Manli Na
Abukar Ali
Veronica Osla
Lindsey Shaw
Wanzhong Wang
Karin Sävman
Elisabet Josefsson
Johan Bylund
Tao Jin
Amanda Welin
Anna Karlsson
Published in Infection and immunity
Volume 85
Issue 7
ISSN 1098-5522
Publication year 2017
Published at Institute of Odontology
Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Clinical Sciences, Department of Pediatrics
Institute of Odontology, Section 3
Language en
Subject categories Immunology in the medical area, Microbiology in the medical area


Staphylococcus aureus is a major cause of skin and soft-tissue infection. The bacterium expresses four major proteases emerging as virulence factors; aureolysin (Aur), V8 protease (SspA), staphopain A (ScpA), and staphopain B (SspB). We hypothesized that human galectin-3, a β-galactoside-binding lectin involved in immune regulation and antimicrobial defense, is a target for these proteases, and that proteolysis of galectin-3 is a novel immune evasion mechanism. Indeed, supernatants from laboratory strains and clinical isolates of S. aureus caused galectin-3 degradation. Similar proteolytic capacity was found in Staphylococcus epidermidis isolates, but not Staphylococcus saprophyticus Galectin-3-induced activation of the neutrophil NADPH-oxidase was abrogated by bacteria-derived proteolysis of galectin-3, and SspB was identified as the major protease responsible. The impact of galectin-3 and protease expression on S. aureus virulence was studied in a murine skin infection model. In galectin-3(+/+) mice, SspB-expressing S. aureus caused larger lesions and higher bacterial load than protease-lacking bacteria. No such difference was detected in galectin-3(-/-) mice, which also showed smaller lesion size as compared to the galectin-3(+/+) animals. In conclusion, the staphylococcal protease SspB inactivates galectin-3, abrogating its stimulation of oxygen radical production in human neutrophils and increasing tissue damage during skin infection.

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