Enterovirus-induced gene expression profile is critical for human pancreatic islet destruction

P. Ylipaasto1, T. Smura1, P. Gopalacharyulu2, A. Paananen1, T. Seppänen-Laakso2, S. Kaijalainen1, H. Ahlfors3,4, O. Korsgren5, J. R. T. Lakey6, R. Lahesmaa4, L. Piemonti7, M. Oresic2, J. Galama, M. Roivainen1
1Intestinal Viruses Unit, National Institute for Health and Welfare (THL), Helsinki, Finland
2VTT Technical Research Center of Finland, Espoo, Finland
3Division of Molecular Immunology, MRC National Institute for Medical Research, London, UK
4Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland
5Division of Clinical Immunology, Department of Oncology, Radiology, and Clinical Immunology, The Rudbeck Laboratory, Uppsala University, Uppsala, Sweden
6Department of Surgery, University of California, Irvine, USA
7Diabetes Research Institute (HSR-DRI), San Raffaele Scientific Institute, Milan, Italy

Tóm tắt

Virally induced inflammatory responses, beta cell destruction and release of beta cell autoantigens may lead to autoimmune reactions culminating in type 1 diabetes. Therefore, viral capability to induce beta cell death and the nature of virus-induced immune responses are among key determinants of diabetogenic viruses. We hypothesised that enterovirus infection induces a specific gene expression pattern that results in islet destruction and that such a host response pattern is not shared among all enterovirus infections but varies between virus strains. The changes in global gene expression and secreted cytokine profiles induced by lytic or benign enterovirus infections were studied in primary human pancreatic islet using DNA microarrays and viral strains either isolated at the clinical onset of type 1 diabetes or capable of causing a diabetes-like condition in mice. The expression of pro-inflammatory cytokine genes (IL-1-α, IL-1-β and TNF-α) that also mediate cytokine-induced beta cell dysfunction correlated with the lytic potential of a virus. Temporally increasing gene expression levels of double-stranded RNA recognition receptors, antiviral molecules, cytokines and chemokines were detected for all studied virus strains. Lytic coxsackievirus B5 (CBV-5)-DS infection also downregulated genes involved in glycolysis and insulin secretion. The results suggest a distinct, virus-strain-specific, gene expression pattern leading to pancreatic islet destruction and pro-inflammatory effects after enterovirus infection. However, neither viral replication nor cytotoxic cytokine production alone are sufficient to induce necrotic cell death. More likely the combined effect of these and possibly cellular energy depletion lie behind the enterovirus-induced necrosis of islets.

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