Fecal Fungal Microbiota (Mycobiome) Study as a Potential Tool for Precision Medicine in Inflammatory Bowel Disease.

There is growing evidence of the role of fungal microbiota in the pathogenesis of inflammatory bowel disease (IBD). Fungi can exert direct pro-inflammatory effects or modify the bacterial composition via interkingdom interactions. Although several studies have demonstrated alterations in the fecal fungal microbiota composition in IBD, there is a wide variation in the mycobiome in different populations, with no definite pattern that can define the mycobiome in IBD having yet been identified. Recent work has suggested that characterizing the fecal fungal composition may influence therapeutic decisions and help to predict outcomes in a subset of IBD patients. In this study, we review the current literature on the emerging role of the fecal mycobiome as a potential tool for precision medicine in IBD.

A Vaccine Based on Kunitz-Type Molecule Confers Protection Against Fasciola hepatica Challenge by Inducing IFN-γ and Antibody Immune Responses Through IL-17A Production.

Fasciola hepatica is helminth parasite found around the world that causes fasciolosis, a chronic disease affecting mainly cattle, sheep, and occasionally humans. Triclabendazole is the drug of choice to treat this parasite. However, the continuous use of this drug has led to the development of parasite resistance and, consequently, the limitation of its effectiveness. Hence, vaccination appears as an attractive option to develop. In this work, we evaluated the potential of F. hepatica Kunitz-type molecule (FhKTM) as an antigen formulated with a liquid crystal nanostructure formed by self-assembly of 6-O-ascorbyl palmitate ester (Coa-ASC16) and the synthetic oligodeoxynucleotide containing unmethylated cytosine-guanine motifs (CpG-ODN) during an experimental model of fasciolosis in mice, and we further dissected the immune response associated with host protection. Our results showed that immunization of mice with FhKTM/CpG-ODN/Coa-ASC16 induces protection against F. hepatica challenge by preventing liver damage and improving survival after F. hepatica infection. FhKTM/CpG-ODN/Coa-ASC16-immunized mice elicited potent IFN-γ and IL-17A with high levels of antigen-specific IgG1, IgG2a, and IgA serum antibodies. Strikingly, IL-17A blockade during infection decreased IgG2a and IgA antibody levels as well as IFN-γ production, leading to an increase in mortality of vaccinated mice. The present study highlights the potential of a new vaccine formulation to improve control and help the eradication of F. hepatica infection, with potential applications for natural hosts such as cattle and sheep.