Figure 2. Differential activity of human beta-defensins against candidal species. (A–F) Human beta defensin killing of candidal species. Recombinant hBD-1, -2, and -3 were incubated at increasing concentrations (0–10 µM) with strains of C. albicans (OPC76, OPC84; OPC99; SC5314), C. krusei (A91, MRL-214), C. parapsilosis (A58, ATCC 22019), and C. glabrata (90030, 2255), respectively, 37°C, 3 hrs, followed by serial dilutions, plating on Sabouraud Dextrose agar plates, and counting of colonies 48 hrs later. (A) rhBD-1 killing of C. albicans strains; (B) rhBD-1 killing of Candida krusei, C. parapsilosis, and C. glabrata strains; (C) rhBD-2 killing of C. albicans strains; (D) rhBD-2 killing of Candida krusei, C. parapsilosis, and C. glabrata strains; (E) rhBD-3 killing of C. albicans strains; and (F) rhBD-3 killing of Candida krusei, C. parapsilosis, and C. glabrata strains. Results are calculated as a percentage of colony-forming units when compared with untreated controls. Data are presented as mean ± SD of 3 (n = 3) independent experiments. (G,H) ß-defensin inhibition of Candida glabrata adherence to human oral epithelial cells. C. glabrata strain 90030 (G) or C. glabrata strain 2255 (H) was incubated with either rhBD-1, -2, or -3 (2.5 or 5 µM), at 37°C, for 3 hrs, followed by assay for adherence to confluent monolayers of OKF6/Tert cells. Results are calculated as a percentage of adhering fungi when compared with untreated controls. Data are presented as mean ± SD of 3 (n = 3) independent experiments. Asterisks show a significant difference from control values at *P < 0.05 and **P < 0.005 by Student’s unpaired t test.