UDC: 616.94:576.8.06:616.155.34:616.155.321]-002.828-092.9

   Background. Sepsis is a major global health problem, with fungal pathogens such as Candida albicans emerging as a significant cause of invasive infection. Fungal sepsis has a higher mortality rate than bacterial sepsis and is complicated by antifungal resistance. Although neutrophil extracellular traps (NETs) help to contain fungi, excessive NETs can contribute to inflammation and tissue injury. Understanding these mechanisms could reveal markers of disease activity and new therapeutic targets. Materials and Methods. Fungal sepsis was induced in twelve male BALB/c mice via an intraperitoneal injection of Meyerozyma guilliermondii (107 cells per mouse). Blood was collected at the beginning of the study and then on days 1–3, 7–9, and 13–15. Serum was analyzed for IgG, IgM, circulating immune complexes (ELISA), and extracellular DNA (fluorescence assay). 
   Results and Discussion. In mice with fungal sepsis, IgG levels remained stable while IgM levels increased significantly between days 7 and 9, before declining from day 13. IgG–IgM immune complexes peaked around days 8–9, reflecting active antigenantibody responses. Free DNA levels, which indicate NETs formation, increased by day 7 and then declined, showing early neutrophil activation followed by humoral control. Together, these findings suggest a coordinated immune response in which NETs and immune complexes contribute to both pathogen control and inflammation.
   Conclusion. Fungal sepsis induced by Meyerozyma guilliermondii resulted in early NETosis and an increase in IgM and immune complexes. IgM levels peaked on days 7–9 before declining. Unlike Candida albicans, this strain does not cause rapid lethality, enabling detailed tracking of disease progression over time. After day 9, immune parameters began to normalize, indicating the resolution of the acute phase and supporting the usefulness of this model for studying host immune dynamics in fungal sepsis.
   Keywords: fungal sepsis, Meyerozyma guilliermondii, acute inflammation, immune defense, circulating immune complexes, neutrophil extracellular traps
(NETs)