Galectin-3 enhances neutrophil motility and extravasation into the airways during Aspergillus fumigatus infection.

ABSTRACT: Aspergillus fumigatus is an opportunistic mold that infects patients who are immunocompromised or have chronic lung disease, causing significant morbidity and mortality in these populations. While the factors governing the host response to A. fumigatus remain poorly defined, neutrophil recruitment to the site of infection is critical to clear the fungus. Galectin-3 is a mammalian β-galactose-binding lectin with both antimicrobial and immunomodulatory activities, however the role of galectin-3 in the defense against molds has not been studied. Here we show that galectin-3 expression is markedly up-regulated in mice and humans with pulmonary aspergillosis. Galectin-3 deficient mice displayed increased fungal burden and higher mortality during pulmonary infection. In contrast to previous repo

SUBMITTER: Snarr BD 

PROVIDER: S-EPMC7428289 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature