Effect of interleukin-17 on in vitro cytokine production in healthy controls and patients with severe sepsis

Interleukin (IL)-17 family members (IL-17A to IL-17F) are appearing to play key roles in host defense and inflammatory disease. Recently, several cytokines, such as IL-6, IL-10, IL-12, and transforming growth factor (TGF)-β1, were shown to have vital roles in severe sepsis. However, the influence of...

Full description

Saved in:
Bibliographic Details
Published inJournal of the Formosan Medical Association Vol. 114; no. 12; pp. 1250 - 1257
Main Authors Wu, Huang-Pin, Shih, Chi-Chung, Chu, Chien-Ming, Huang, Chih-Yu, Hua, Chung-Ching, Liu, Yu-Chih, Chuang, Duen-Yau
Format Journal Article
LanguageEnglish
Published Singapore Elsevier B.V 01.12.2015
Elsevier
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Interleukin (IL)-17 family members (IL-17A to IL-17F) are appearing to play key roles in host defense and inflammatory disease. Recently, several cytokines, such as IL-6, IL-10, IL-12, and transforming growth factor (TGF)-β1, were shown to have vital roles in severe sepsis. However, the influence of IL-17 on these cytokine responses from peripheral blood mononuclear cells (PBMCs) is unclear. Fifty-two patients who were admitted to our intensive care unit (ICU) because of severe sepsis were enrolled into this study. To validate experimental findings, 25 healthy controls were enrolled. Lipopolysaccharide-stimulated PBMCs with IL-17 or anti-IL-17 treatments were cultured for 24 hours. IL-6, IL-10, IL-12, and TGF-β1 levels in supernatants were measured. The IL-12 production from stimulated PBMCs was increased after IL-17 treatment in both control and patient groups. Additional treatment of anti-IL-17 enhanced IL-10 production but decreased IL-12 production from stimulated PBMCs of healthy controls and patients with severe sepsis. IL-17 was helpful for inflammation in severe sepsis. Lack of IL-17 decreased IL-12 and enhanced IL-10 production from PBMCs, which resulted in immune imbalance.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0929-6646
DOI:10.1016/j.jfma.2014.09.009