Invasive Candida infection is one of the leading causes of hospital-acquired bloodstream infections, which carry a mortality rate ranging from 45 to 75 percent. Toxicity and resistance to the limited number of anti-fungal agents currently available contributes to high morbidity and mortality associated with invasive fungal infections. Therefore, there is an urgent need to better understand the host-pathogen interaction during fungal infection and develop new immuno-therapeutic approaches to fight invasive candidiasis.

In a recent article entitled “Akt-2 is a potential therapeutic target for disseminated candidiasis”, the Zhang laboratory first discovered a differential role of Akt isoforms in anti-fungal innate immunity. Interestingly, Akt2–/– , but not Akt1–/–, mice are protected from lethal C. albicans infection. Loss of Akt-2 facilitates the recruitment of neutrophils and macrophages to the spleen, and increases ROS expression in these cells. Treating C57BL/6 mice with a specific inhibitor for Akt-2 but not Akt-1, provides protection from lethal C. albicans infection. Therefore, this study unveils a novel role for Akt-2 in the regulation of anti-fungal innate immunity, indicatingAkt-2 as a potential target for the treatment of fungal sepsis. These findings were published in the September 1 issue of the Journal of Immunology and highlighted by the Editors as a ‘Top Reads’ article.

Ling Huang, M.D., a visiting scholar in Zhang laboratory, is the lead author of the study. Co-authors include Yilei Ma, Hui Guo, Na Tang, Patrick Nuro-Gyina, and Matthew C. O’Brien from the University of Iowa, Song Ouyang and Yusen Liu from the Ohio State University, Lijian Tao from Central South University (China), and Wallace Y. Langdon from the University of Western Australia.

The article can be viewed at:  https://www.jimmunol.org/content/209/5/991.abstract?etoc