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Staphylococcus aureus triggers a protective inflammatory response against secondary Cryptococcus gattii infection in a murine model

2023; Elsevier BV; Volume: 25; Issue: 6 Linguagem: Inglês

10.1016/j.micinf.2023.105122

1769-714X

Elúzia Castro Peres Emídio, Júnya de Lacorte Singulani, Gustavo José Cota de Freitas, Marliete Carvalho da Costa, Ludmila Gouveia‐Eufrásio, Paulo Henrique Fonseca do Carmo, Sílvia Helena Sousa Pietra Pedroso, Camila Bernardo de Brito, Rafael Wesley Bastos, Noelly Queiroz Ribeiro, Lorena V. N. Oliveira, Monique Ferreira Silva, Tatiane A. Paíxão, Danielle G. Souza, Daniel Assis Santos,

Nail Diseases and Treatments

Prior infections can provide protection or enhance susceptibility to a subsequent infection through microorganism's interaction or host immunomodulation. Staphylococcus aureus (SA) and Cryptococcus gattii (CG) cause lungs infection, but it is unclear how they interact in vivo. This study aimed to study the effects of the primary SA lung infection on secondary cryptococcosis caused by CG in a murine model. The mice's survival, fungal burden, behavior, immune cells, cytokines, and chemokines were quantified to evaluate murine cryptococcosis under the influence of a previous SA infection. Further, fungal-bacterial in vitro interaction was studied in a culture medium and a phagocytosis assay. The primary infection with SA protects animals from the subsequent CG infection by reducing lethality, improving behavior, and impairing the fungal proliferation within the host. This phenotype was associated with the proinflammatory antifungal host response elicited by the bacteria in the early stage of cryptococcosis. There was no direct inhibition of CG by SA, although the phagocytic activity of macrophages was reduced. Identifying mechanisms involved in this protection may lead to new approaches for preventing and treating cryptococcosis.