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Mediators of Inflammation
Volume 2015, Article ID 236839, 9 pages
Research Article

Interleukin-18 Increases TLR4 and Mannose Receptor Expression and Modulates Cytokine Production in Human Monocytes

1Departamento de Patologia, Faculdade de Medicina, Universidade Estadual Paulista (UNESP), Campus Botucatu, 18618-970 Botucatu, SP, Brazil
2Departamento de Microbiologia e Imunologia, Instituto de Biociências, Universidade Estadual Paulista (UNESP), Campus Botucatu, 18618-970 Botucatu, SP, Brazil
3Faculdade de Medicina, Universidade Estadual Paulista (UNESP), Campus Botucatu, Hemocentro, 18618-970 Botucatu, SP, Brazil

Received 6 June 2014; Revised 2 September 2014; Accepted 3 September 2014

Academic Editor: Fábio Santos Lira

Copyright © 2015 Luciane Alarcão Dias-Melicio 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.


Interleukin-18 is a proinflammatory cytokine belonging to the interleukin-1 family of cytokines. This cytokine exerts many unique biological and immunological effects. To explore the role of IL-18 in inflammatory innate immune responses, we investigated its impact on expression of two toll-like receptors (TLR2 and TLR4) and mannose receptor (MR) by human peripheral blood monocytes and its effect on TNF-α, IL-12, IL-15, and IL-10 production. Monocytes from healthy donors were stimulated or not with IL-18 for 18 h, and then the TLR2, TLR4, and MR expression and intracellular TNF-α, IL-12, and IL-10 production were assessed by flow cytometry and the levels of TNF-α, IL-12, IL-15, and IL-10 in culture supernatants were measured by ELISA. IL-18 treatment was able to increase TLR4 and MR expression by monocytes. The production of TNF-α and IL-10 was also increased by cytokine treatment. However, IL-18 was unable to induce neither IL-12 nor IL-15 production by these cells. Taken together, these results show an important role of IL-18 on the early phase of inflammatory response by promoting the expression of some pattern recognition receptors (PRRs) that are important during the microbe recognition phase and by inducing some important cytokines such as TNF-α and IL-10.