Galectin-3 inhibits Paracoccidioides brasiliensis growth and impacts Paracoccidioidomycosis through multiple mechanisms

Otavio Hatanaka, Caroline Patini Rezende, Pedro Moreno, Fabrício Freitas Fernandes, Patrícia Kellen Martins Oliveira Brito, Roberto Martinez, Carolina Coelho, Maria Cristina Roque-Barreira, Arturo Casadevall, Fausto Almeida

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


The thermodimorphic pathogenic fungi Paracoccidioides brasiliensis and Paracoccidioides lutzii are the etiologic causes of paracoccidioidomycosis (PCM), the most prevalent systemic mycosis in Latin America. Galectin-3 (Gal-3), an animal galactoside-binding protein, modulates important roles during microbial infections, such as triggering a Th2-polarized immune response in PCM. Herein, we demonstrate that Gal-3 also plays other important roles in P. brasiliensis infection. We verified that Gal-3 levels are upregulated in human and mice infections and established that Gal-3 inhibited P. brasiliensis growth by inhibiting budding. Furthermore, Gal-3 affected disruption and internalization of extracellular vesicles (EVs) from P. brasiliensis by macrophages. Our results suggest important protective roles for Gal-3 in P. brasiliensis infection, indicating that increased Gal-3 production during P. brasiliensis infection may affect fungal growth and EV stability, thus promoting beneficial effects that could influence the course of PCM. The finding that Gal-3 has effects against P. brasiliensis together with previously reported effects against Cryptococcus neoformans suggests that molecule has a general antifungal role in innate defenses against fungal pathogens.

Original languageEnglish (US)
Article numbere00209-19
Issue number2
StatePublished - Mar 1 2019


  • Extracellular vesicles
  • Fungal infection
  • Galectin-3
  • Paracoccidioides brasiliensis

ASJC Scopus subject areas

  • Microbiology
  • Molecular Biology


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