Candida albicans: The Ability to Invade Epithelial Cells and Survive under Oxidative Stress Is Unlinked to Hyphal Length

Autor(es):Mostrar menos -

Maza, Paloma K. ; Bonfim-Melo, Alexis ; Padovan, Ana C. B. ; Mortara, Renato A. ; Orikaza, Cristina M. ; Damas Ramos, Lilian M. ; Moura, Tauany R. ; Soriani, Frederico M. ; Almeida, Ricardo S. ; Suzuki, Erika ; Bahia, Diana

• Tipo de documento: Artigo Científico
• Fonte: FRONTIERS IN MICROBIOLOGY; v. 8, JUL 17 2017.
• Citações Web of Science: 0

Resumo

In its hyphal form, Candida albicans invades epithelial and endothelial cells by two distinct mechanisms: active penetration and induced endocytosis. The latter is dependent on a reorganization of the host cytoskeleton (actin/cortactin recruitment), whilst active penetration does not rely on the host's cellular machinery. The first obstacle for the fungus to reach deep tissues is the epithelial barrier and this interaction is crucial for commensal growth, fungal pathogenicity and host defense. This study aimed to characterize in vitro epithelial HeLa cell invasion by four different isolates of C. albicans with distinct clinical backgrounds, including a C. albicans SC5314 reference strain. All isolates invaded HeLa cells, recruited actin and cortactin, and induced the phosphorylation of both Src-family kinases (SFK) and cortactin. Curiously, L3881 isolated from blood culture of a patient exhibited the highest resistance to oxidative stress, although this isolate showed reduced hyphal length and displayed the lowest cell damage and invasion rates. Collectively, these data suggest that the ability of C. albicans to invade HeLa cells, and to reach and adapt to the host's blood, including resistance to oxidative stress, may be independent of hyphal length. (AU)

• Processo FAPESP: 15/25652-6 - Estudo da comunicação entre receptores e suas vias de sinalização na secreção de citocinas, induzida por fungos em células epiteliais
• Beneficiário: Erika Suzuki de Toledo
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 11/22773-6 - Estudos sobre os mecanismos de adesão e modulação de citocinas durante a interação entre células epiteliais e fungos patogênicos
• Beneficiário: Erika Suzuki de Toledo
• Modalidade de apoio: Auxílio à Pesquisa - Regular