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Copyright © 2013 Helen Rogers et al. Helen Rogers et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Human infections involving yeast of the genus Candidaoften occur in the presence of bacteria, and, as such, it is important to understand how these bacteria influence innate host immunity towards Candida. Dectin-1 is a cell receptor of macrophages for Candida albicansrecognition. The aim of this study was to examine dectin-1 expression by monocytes after stimulation with bacterial lipopolysaccharide (LPS), followed by heat-killed C. albicans(HKC). Freshly isolated human peripheral blood monocytes (PBMCs) and human monocytes cell line (THP-1) cells expressed low levels of dectin-1. Stimulation with LPS and GM-CSF/IL-4 was found to increase dectin-1 expression in both CD14+human PBMC and THP-1 cells. Enhanced dectin-1 expression resulted in increased phagocytosis of Candida. When THP-1 cells were challenged only with HKC, detectable levels of IL-23 were not evident. However, challenge by LPS followed by varying concentrations of HKC resulted in increased IL-23 expression by THP-1 cells in HKC dose-dependent manner. Increased expression of IL-17 by PBMC also occurred after stimulation with Candidaand LPS. In conclusion, bacterial LPS induces an enhanced immune response to Candidaby immune cells, and this occurs through increasing dectin-1 expression.

Details

Title
Role of Bacterial Lipopolysaccharide in Enhancing Host Immune Response to Candida albicans
Author
Rogers, Helen; Williams, David W; Gui-Jie Feng; Lewis, Michael A O; Xiao-Qing, Wei
Pages
320168
Publication year
2013
Publication date
2013
Publisher
John Wiley & Sons, Inc.
ISSN
17402522
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
1419990418
Copyright
Copyright © 2013 Helen Rogers et al. Helen Rogers et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.