COST Action 23142 at TIMM-12: From Antifungal Resistance to Host Immunity in Pneumocystis
At TIMM-12, COST Action 23142 Delve-into-Pneumocystis members Dr. Solène Le Gal, Dr. Rocío Salsoso, and Dr. Elena Charpentier shared their latest findings, highlighting advances in antifungal resistance, host genetics, and maternal-infant immunity in Pneumocystis jirovecii.
COST Action 23142 Delve into Pneumocystis was strongly represented at the 12th Trends in Medical Mycology (TIMM-12), where three members showcased complementary research advancing our understanding of Pneumocystis jirovecii across different clinical and immunological contexts.
Dr. Solène Le Gal participated as an invited speaker in a session dedicated exclusively to Pneumocystis. Her lecture addressed the potential antifungal activity of calcineurin inhibitors against P. jirovecii. Given that solid organ transplant (SOT) recipients are at high risk of Pneumocystis pneumonia (PCP) due to immunosuppressive therapy, her research highlights how commonly used drugs such as mycophenolic acid, ciclosporin, or tacrolimus, beyond their immunosuppressive roles, may exert selective pressure on the fungus. Previous findings identified specific mutations in the impdh gene of P. jirovecii isolates from treated patients, suggesting a potential link between drug exposure and fungal resistance. Ongoing investigations now focus on the diversity of genes encoding immunophilins in P. jirovecii to assess whether similar selective pressures may arise from calcineurin inhibitor treatments.
Dr. Rocío Salsoso presented a poster on the role of host genetic polymorphisms in shaping the inflammatory response to P. jirovecii colonisation in patients with severe chronic obstructive pulmonary disease (COPD). Among 42 patients examined, colonisation was detected in 40.5% and was associated with significantly increased systemic levels of pro-inflammatory cytokines such as IL-6, TNF-α, IL-8, IL-1α, and IL-2, alongside reduced IL-10. Importantly, an IL-6 gene polymorphism (rs1800795 GG genotype) correlated with higher IL-6 levels in colonised patients, underscoring the role of host genetics in modulating inflammatory outcomes. These findings confirm that P. jirovecii colonisation exacerbates systemic inflammation in COPD and that patient-specific genetic backgrounds may influence the magnitude of this response.
Dr. Elena Charpentier presented a poster reporting on a prospective study of maternal immunity and vertical transmission of P. jirovecii in premature births. Conducted at the University Hospital of Seville, this research confirmed that pregnant women are particularly susceptible to colonisation (51.8% vs. 16.7% in controls). Colonised mothers exhibited reduced levels of anti-Kex1 IgM antibodies, particularly during summer births, suggesting a seasonal modulation of immune responses. Nearly half of colonised mothers had newborns who were also colonised at birth, with maternal age, primiparity, and lower total IgG levels identified as risk factors. The study underscores how maternal humoral immunity, and especially IgM and IgG dynamics, may shape both maternal colonisation and the likelihood of transmission to infants, with potential implications for neonatal respiratory health.
Together, these three contributions illustrate the multidisciplinary efforts within COST Action 23142 to address P. jirovecii from multiple perspectives: antifungal resistance, host genetic susceptibility, and maternal–infant immunity. The active participation of our members at TIMM-12, through both invited lectures and poster presentations, highlights the commitment of our network to fostering collaborative research and advancing knowledge on this medically significant opportunistic fungus.
