Extracellular vesicles from diverse fungal pathogens induce species-specific and endocytosis-dependent immunomodulation.

Microbial pathogens generate extracellular vesicles (EVs) for intercellular communication and quorum sensing. Microbial EVs also induce inflammatory pathways within host innate immune cells. We previously demonstrated that EVs secreted by trigger type I interferon signaling in host cells specifically via the cGAS-STING innate immune signaling pathway.

Interactions of the emerging fungus with reveal phenotypic changes with direct implications on the response to stress and virulence.

Unlabelled: is an emerging fungal pathogen notable for its resistance to multiple antifungals and ability to survive in various environments. Understanding the interactions between and environmental protozoa, such as could provide insights into fungal adaptability and pathogenicity. Two isolates (MMC1 and MMC2) were co-cultured with to examine interaction dynamics, survival, stress responses, growth, virulence, biofilm formation, and antifungal susceptibility.

The biofilm produced by Cryptococcus neoformans protects the fungus from the antifungal and anti-melanin effects of cyclosporine.

Understanding Cryptococcus neoformans pathogenesis requires a detailed analysis of the various virulence factors that contribute to its ability to cause disease. Cyclosporine, calcineurin inhibitor, impairs C. neoformans production of a polysaccharide capsule and secretion of urease, which are critical for cryptococcal pathogenesis.

Alkaloids solenopsins from fire ants display and activity against the yeast .

The urgency surrounding as a public health threat is highlighted by both the Center for Disease Control (CDC) and World Health Organization (WHO) that categorized this species as a priority fungal pathogen. Given the current limitations of antifungal therapy for , particularly due to its multiple resistance to the current antifungals, the identification of new drugs is of paramount importance. Some alkaloids abundant in the venom of the red invasive fire ant (), known as solenopsins, have garnered attention as potent inhibitors of bacterial biofilms, and there are no studies demonstrating such effects against fungal pathogens.

The microbial damage and host response framework: lesson learned from pathogenic survival trajectories and immunoinflammatory responses of infection.

The adverse outcomes of fungal infection in mammalian hosts depend on the complex interactions between the host immune system and pathogen virulence-associated traits. The main clinical problems arise when the host response is either too weak to effectively eliminate the pathogen or overly aggressive, resulting in host tissue damage rather than protection. This article will highlight current knowledge regarding the virulence attributions and mechanisms involved in the dual-sided role of the host immune system in the immunopathogenesis of the thermally dimorphic fungus through the lens of the damage response framework (DRF) of microbial pathogenesis model.