Single-cell RNA sequencing analysis of spleen immune cell changes in mice infected systemically with wild-type or FASN-alpha subunit deletion Candida albicans strains

This study uses single-cell RNA sequencing (scRNA-seq) to investigate the immune cell response in the spleen of mice systemically infected with either wild-type (WT) Candida albicans or FASN-alpha deletion mutants. The goal is to characterize the immune cell changes, activation states, and transcriptional profiles induced by the infection with the FASN-alpha-deficient strains as compared to the WT strain, both before and after the secondary immune challenge. We hypothesize that the FASN-alpha deletion will lead to distinct immune responses, potentially altering immune cell activation, recruitment, and differentiation in the spleen. This study will use a mouse model of systemic Candida albicans infection. Mice will be infected with either WT Candida albicans or a FASN-alpha deletion mutant strain. After initial infection, mice will undergo a secondary infection challenge with WT Candida albicans to simulate a reinfection scenario. Spleen cells will be harvested at different time points following infection and challenged with the secondary infection. We will then perform single-cell RNA sequencing to capture the transcriptomic profile of individual immune cells. This will allow for a detailed investigation of immune cell activation, differentiation, and functional changes in response to infection with the FASN-alpha deletion strain versus the WT strain. This study is expected to provide novel insights into the role of FASN-alpha in shaping host immune responses during systemic Candida albicans infection. Understanding how FASN-alpha deletion alters immune cell dynamics at the single-cell level could reveal new mechanisms of immune evasion and potentially highlight novel therapeutic targets for enhancing immune responses against fungal infections. By leveraging single-cell RNA sequencing, we can gain a more granular understanding of the immune response, which could inform strategies for improving antifungal therapies and vaccine development.