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Updated: May 6, 2026
Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates
Published on: July 6, 2013
Comprehensive Analysis of Soluble Mediator Profiles in Congenital CMV Infection Using an MCMV Model
Dubravka Karner1, Daria Kvestak1, Berislav Lisnic1
1Center for Proteomics, Faculty of Medicine, University of Rijeka, 51000 Rijeka, Croatia.
Abstract:
Congenital human cytomegalovirus (HCMV) infection may cause life-threatening disease and permanent damage to the central nervous system. The mouse model of CMV infection is most commonly used to study mechanisms of infection and pathogenesis. While essential to limit mouse CMV (MCMV) replication, the inflammatory responses, particularly IFNγ and TNFα, cause neurodevelopmental abnormalities. Other soluble mediators of the immune response in most tissues remain largely unexplored. To address this gap, we quantified 48 soluble mediators of the immune response, including 32 cytokines, 10 chemokines, 3 growth factors/regulators, and 3 soluble receptors in the spleen, liver, lungs, and brain at 9 and 14 days postinfection (dpi). Our analysis found 25 induced molecules in the brain at 9 dpi, with an additional 8 showing statistically elevated responses at 14 dpi. Specifically, all analyzed CCL group cytokines (CCL2, CCL3, CCL4, CCL5, CCL7, and CCL11) were upregulated at 14 dpi in the brain. Furthermore, data revealed differentially regulated analytes across tissues, such as CCL11, CXCL5, and IL-10 in the brain, IL-33/IL-33R in the liver, and VEGF-a and IL-5 in the lungs. Overall, this study provides an overview of the immune dynamics of soluble mediators in congenital CMV.
Insights
Congenital human cytomegalovirus (HCMV) infection impacts the brain, with immune responses involving cytokines and chemokines. This study maps these soluble mediators in the brain and other organs during MCMV infection.
Area of Science:
- Immunology
- Virology
- Neuroscience
Background:
- Congenital human cytomegalovirus (HCMV) infection can lead to severe disease and lasting neurological damage.
- The mouse model is crucial for studying CMV infection mechanisms and pathogenesis.
- Inflammatory responses, like IFNγ and TNFα, in MCMV infection cause neurodevelopmental issues, but other immune mediators are less understood.
Purpose of the Study:
- To comprehensively analyze the profile of soluble immune mediators in various tissues during congenital CMV infection.
- To identify specific immune molecules and their dynamics in the brain following infection.
- To understand the broader immune response landscape beyond key inflammatory cytokines.
Main Methods:
- Quantification of 48 soluble immune mediators (cytokines, chemokines, growth factors, soluble receptors) using multiplex assays.
- Analysis of spleen, liver, lungs, and brain tissues at 9 and 14 days postinfection (dpi).
- Statistical analysis to identify significantly upregulated or differentially regulated mediators across tissues and time points.
Main Results:
- 25 immune mediators were induced in the brain by 9 dpi, with 8 additional molecules elevated by 14 dpi.
- All tested CCL chemokines (CCL2, CCL3, CCL4, CCL5, CCL7, CCL11) were upregulated in the brain at 14 dpi.
- Tissue-specific regulation observed for mediators like CCL11, CXCL5, IL-10 (brain), IL-33/IL-33R (liver), and VEGF-a, IL-5 (lungs).
Conclusions:
- This study provides a detailed overview of soluble immune mediator dynamics in the context of congenital CMV infection.
- Identified specific chemokines and cytokines that are significantly upregulated in the brain during infection.
- Highlights differential immune responses across various organs, offering insights into pathogenesis and potential therapeutic targets.
