IADR Abstract Archives
Candida albicans up-regulates synthetic bacterial components-induced proinflammatory cytokine production.
Objectives: It has been reported that Candida albicans enhanced invasion of oral epithelial cells by Porphyromonas gingivalis although the fungus is not a periodontalpathogen. C. albicans is recognized by many receptors, such as Toll-like receptor (TLR) 2, TLR4, dectin-1 and dectin-2 and can cause sepsis by bloodstream infections in immunocompromised hosts. In this study, we investigated whether C. albicans augmented proinflammatory cytokine production by mouse macrophage-like J774.1 cells incubated with synthetic bacterial components.
Methods: C. albicans was heat-killed (95°C, 30m). Mouse macrophage-like J774.1 cells (2×105cells/well) were pretreated with or without heat-killed C. albicans or the substitutes for C. albicans cell wall components in 96-well flat-bottomed plates (37°C, 3h). Cells were then washed and incubated with 100ng/ml Pam3CSK4, a Toll-like receptor (TLR) 2 ligand, or 100ng/ml lipid A, a TLR4 ligand (37°C, 24h). The culture supernatants were analyzed by ELISA for secreted mouse IL-6, MCP-1, and TNF-α. Data were statistically analyzed (ANOVA, Bonferroni or Dunn, p<0.05).
Results: Heat-killed C. albicans up-regulated TLR ligands-induced proinflammatory cytokine production by J774.1 cells. However, pretreatment of the cells with curdlan, a dectin-1 ligand, did not augment IL-6, MCP-1, and TNF-α production induced by Pam3CSK4 or lipid A.
Conclusions: Candida albicans up-regulates synthetic bacterial components-induced cytokine production via TLR pathway not dectin-1 pathway by J774.1 cells.
Methods: C. albicans was heat-killed (95°C, 30m). Mouse macrophage-like J774.1 cells (2×105cells/well) were pretreated with or without heat-killed C. albicans or the substitutes for C. albicans cell wall components in 96-well flat-bottomed plates (37°C, 3h). Cells were then washed and incubated with 100ng/ml Pam3CSK4, a Toll-like receptor (TLR) 2 ligand, or 100ng/ml lipid A, a TLR4 ligand (37°C, 24h). The culture supernatants were analyzed by ELISA for secreted mouse IL-6, MCP-1, and TNF-α. Data were statistically analyzed (ANOVA, Bonferroni or Dunn, p<0.05).
Results: Heat-killed C. albicans up-regulated TLR ligands-induced proinflammatory cytokine production by J774.1 cells. However, pretreatment of the cells with curdlan, a dectin-1 ligand, did not augment IL-6, MCP-1, and TNF-α production induced by Pam3CSK4 or lipid A.
Conclusions: Candida albicans up-regulates synthetic bacterial components-induced cytokine production via TLR pathway not dectin-1 pathway by J774.1 cells.