Fig. 4: Reduced innate immune response to C. auris is morphology-independent and functionally conserved.

a Production of TNF-α, IL-6, IL-1β, CXCL1, and CXCL2, as determined by ELISA, in the culture supernatants of BMDM that were stimulated without (PBS) or with the yeast (Y), filamentation-competent (FC) yeast or filamentous (F) form of C. auris BJCA001 (MOI = 5) for 6 h (n = 3). b, c Shown are the major immune cell populations in spleen (b) and kidney (c) cell suspensions of mice that were infected without (PBS, negative control) or with the yeast (Y; n = 5) or filamentation-competent (FC; n = 5) yeast form of C. auris BJCA001 for 2 and 5 days. C. auris was injected into mice at an inoculum of 1× 10⁶ CFU (L). d Serum cytokine and chemokine levels were determined by ELISA, using mice treated as in b, c. e–g The innate immune response against various fluconazole-resistant clinical isolates of C. auris. e Expression of IL-1β, IL-6, TNF-α, CXCL1 and CXCL2 were analyzed by real-time RT-qPCR. BMDMs were stimulated without (PBS control) or with each of the eleven fluconazole-resistant clinical isolates of C. auris or C. albicans SC5314 at MOI = 5 for 3 h. Results were normalized to the expression of the control gene GAPDH and are presented relative to those of negative control, set as 1. f Production of the cytokines and chemokines were analyzed by ELISA after BMDMs were stimulated with indicated strains at MOI = 5 for 6 h (n = 3). g Similar to f, except for lower inoculum of C. auris (MOI = 0.1) and longer stimulation time (24 h). Data are expressed as mean ± SD and are representative of three independent experiments. ns, no significance; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; by one-way ANOVA with Sidak’s test (a, d–g) or two-way ANOVA with Tukey’s test (b, c). Source data are provided as a Source Data file.