Heat-killed Candida albicans augments synthetic bacterial component-induced proinflammatory cytokine production

• Published in: Folia microbiologica 2019-07, Vol.64 (4), p.555-566
• Main Authors: Tamai, Riyoko, Kiyoura, Yusuke
• Format: Article
• Language: English
• Subjects: Applied Microbiology; Bacteria; Biomedical and Life Sciences; Candida albicans; Cell culture; Cell walls; Cytokines; Environmental Engineering/Biotechnology; Enzyme-linked immunosorbent assay; Epithelial cells; Fungi; Immune system; Immunology; Inflammation; Interleukin 6; Interleukin 8; Life Sciences; Ligands; Lipid A; Lipids; Macrophages; Mannan; Microbiology; Monocyte chemoattractant protein 1; Original Article; Periodontics; Pretreatment; Proteins; Splenocytes; TLR4 protein; Toll-like receptors; Tumor necrosis factor-α
• ISSN: 0015-5632; 1874-9356
• DOI: 10.1007/s12223-019-00679-2

Candida albicans can enhance the invasion of oral epithelial cells by Porphyromonas gingivalis , although the fungus is not a periodontal pathogen. In this study, we investigated whether C. albicans augments proinflammatory cytokine production by mouse macrophage-like J774.1 cells incubated with synthetic bacterial components. Mouse macrophage-like J774.1 cells, mouse primary splenocytes, human THP-1 cells, and A549 cells were pretreated with or without heat-killed C. albicans (HKCA) or substitutes for C. albicans cell wall components in 96-well flat-bottomed plates. Cells were then washed and incubated with Pam 3 CSK 4 , a Toll-like receptor (TLR) 2 ligand, or lipid A, a TLR4 ligand. Culture supernatants were analyzed by ELISA for secreted IL-6, MCP-1, TNF-α, and IL-8. HKCA augmented TLR ligand-induced proinflammatory cytokine production by J774.1 cells, mouse splenocytes, and THP-1 cells, but not A549 cells. However, IL-6, MCP-1, and TNF-α production induced by Pam 3 CSK 4 or lipid A was not augmented when cells were pretreated with curdlan, a dectin-1 ligand, or mannan, a dectin-2 ligand. In contrast, pretreatment of cells with TLR ligands upregulated the production of IL-6 and TNF-α, but not MCP-1, induced by Pam 3 CSK 4 or lipid A. The results suggest that C. albicans augments synthetic bacterial component-induced cytokine production by J774.1 cells via the TLR pathway, but not the dectin-1 or dectin-2 pathway.