High TNF-alpha and IL-8 levels predict low blood dendritic cell counts in primary cytomegalovirus infection

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• 作者：Stefania Varani^a ; ^{stefania.varani@unibo.it} ; Giada Rossini^a ; Antonio Mastroianni^b ; Charlotte Tammik^c ; Giada Frascaroli^d ; Maria Paola Landini^a ; Gastone Castellani^e ; Cecilia S&ouml ; derberg-Nauclé ; r^c
• 关键词：CMV ; human cytomegalovirus ; DC ; dendritic cell ; TNF-伪 ; tumor necrosis factor-伪 ; APC ; antigen presenting cell ; mDC ; myeloid dendritic cell ; pDC ; plasmacytoid dendritic cell ; IFN ; interferon ; CCR ; chemokine receptor ; ALT ; alanine aminotransferase ; AST ; as
• 刊名：Journal of Clinical Virology
• 出版年：2012
• 期刊代码：150_13866532
• 类别：med
• 出版时间：April, 2012
• 卷：53
• 期：4
• 页码：360-363
• 文件大小：401 K

摘要

Background

In vitro studies suggest that human cytomegalovirus (CMV) modulates the functions of dendritic cells (DCs). However, there are limited data on DC homeostasis in CMV-infected patients.

Objectives

The aim of this study was to characterize circulating DCs and plasma cytokine levels in immunocompetent patients with primary, symptomatic CMV infections.

Study design

The study population consisted of 14 patients suffering of CMV mononucleosis and 14 healthy volunteers (11 CMV-seropositive and 3 CMV-seronegative subjects) included as controls. Peripheral blood mononuclear cells were isolated and used to characterize DCs and to quantify CMV in the blood. Plasma levels of pro-inflammatory and anti-inflammatory cytokines were also measured.

Results

We observed that patients who were developing CMV mononucleosis presented lower myeloid and plasmacytoid DC counts in peripheral blood compared with healthy controls. We also noted elevated levels of inflammatory mediators, of which tumor necrosis factor-伪 (TNF-伪)鈥攚hich activates DCs and endothelial cells鈥攚as the highest. Notably, the decrease in blood DCs correlated with high TNF-伪 and IL-8 levels by a hyperbolic function.

Conclusions

Our results suggest that increased levels of inflammatory factors facilitate alterations in DC homeostasis during primary CMV infection, which may contribute to viral-induced modulation of host immunity.