GLUT3 as an Intersection of Glycerophospholipid Metabolism and the Innate Immune Response to Candida albicans

Immune cells can optimize the management of metabolic resources to balance their energy requirements in order to regulate immune responses. The interconnection between immunometabolism and fungal infections is becoming increasingly apparent. Using proteome and metabolome assays, we found that stimulation of primary human monocytes by Candida albicans was accompanied by upregulation of glucose transporter 3 (GLUT3) and activation of the glycerophospholipid metabolism pathway. Upregulated GLUT3 expression has been preliminarily confirmed in monocytes from patients with C. albicans bloodstream infection. Our findings support the importance of GLUT3 in the complex network of glycerophospholipid metabolism and the innate immune responses against C. albicans. In summary, this study might contribute to decipher the regulatory mechanism between the monocyte metabolic reprogramming and innate immune response and reveal potential targets for the antifungal treatments.

Automated summary

This study reveals that stimulation of primary human monocytes by Candida albicans leads to upregulation of GLUT3 and activation of the glycerophospholipid metabolism pathway. Upregulated GLUT3 expression was also observed in monocytes from patients with C. albicans infection. These findings support the importance of GLUT3 in glycerophospholipid metabolism and innate immune responses against fungi.