Severe burn patients are immunodeficient and highly susceptible to infection of Candida albicans, a fungus that causes an opportunistic infection of the skin and mucosal membranes. Fungal infections can be attributed to 33% of mortality among patients with total body surface area (TBSA) burns. Above all, C.albicans infection results in the highest percentage of TBSA patient deaths [1].
Resistance against C.albicans infection is largely attributed to the anti-fungal activities of IL-17 producing CD4 T cells, or Th17 cells. Upon activation, CD4 T cells differentiate into three subsets of T helper cells; Th1, Th2, and Th17. Each type of Th cell produces a unique collection of cytokines, or chemical messengers, which activate different varieties of immune responses [2]. Th17 cells predominantly secrete IL-17, which is essential for mediating host defenses in mucosal surfaces such as the lungs and gut. Past research has implicated IL-17 in the regulation of neutrophils, which are leukocytes involved in the rapid responses of the innate immunity [3]. Specifically, IL-17 recruits neutrophils to a site of infection and enhances the function of epithelial cells, endothelial cells, and macrophages to produces pro-inflammatory cytokines [1]. Previous research implicates IL-17 deficiency in C.albicans infection and chronic mucocutaneous candidasis and demonstrates the necessity of IL-17 to combat fungal infections.
In the present study Inatsu and colleagues attempt to generate Th17 cell cultures in the presence of severely burned patient PBMC (peripheral blood mononuclear cells). PBMC are blood cells with a round nucleus such as monocytes and macrophages [4]. Prior to culture, patient’s PBMC were stimulated by C.albicans antigen (CAg), a protein derived from the fungus that can bind to a cell surface receptor and result in lymphocyte activation. The rationale was that CAg activated cells will be stimulated to produce Th17 cells and IL-17. Ultimately, Th17 were not detected in the cell cultures of CAg activated PBMC. Inatsu and colleagues hypothesis that IL-10, a cytokine detected in the sample of burn patient PBMC, inhibits the generation of Th17 cells and contributes to the increased susceptibility of TBSA individuals to C.albicans.
