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Chronic enteroviral infection modifies broadly pancreatic cellular functions

Date:
September 10, 2019
Source:
University of Turku
Summary:
Enteroviral infections are common viral infections with usually rather few symptoms and also believed to be linked to the onset of type 1 diabetes. Type 1 diabetes is a disorder in which the pancreatic insulin-producing beta-cells are destroyed. A new study supports the link between enteroviral infections and type 1 diabetes.
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Enteroviral infections are common viral infections with usually rather few symptoms and also believed to be linked to the onset of type 1 diabetes. Type 1 diabetes is a disorder in which the pancreatic insulin-producing beta-cells are destroyed, and it is more common in Finland than anywhere else in the world. A new study by the University of Turku and Tampere University in Finland supports the link between enteroviral infections and type 1 diabetes.

The goal of the new study by the research groups of Academy Professor at Turku Bioscience Centre Riitta Lahesmaa and Professor at Tampere University Heikki Hyöty was to understand the mechanisms that control the development of chronic enteroviral infection in the pancreas. The study also aimed at creating a comprehensive picture on the alterations caused by enteroviral infection that could possibly have adverse health effects.

In the study, cutting-edge proteomic methods were utilised to measure how the infection influences the expression and secretion of thousands of different proteins in the cellular models of chronic pancreatic enteroviral infection.

Having persisted for almost a year, the chronic enteroviral infections modified the cellular expression of numerous proteins that are key to cellular functions, such as proteins regulating energy metabolism. The infections also caused alterations in the secretion of several proteins.

"For example, the levels of proteins in the regulated secretory pathway participating in the secretion of hormones such as insulin in the beta-cells decreased with the chronic infection. The infections also clearly affected the levels of other proteins that are involved in the function and survival of beta-cells," says Dr Niina Lietzén from the Turku Bioscience Centre.

"Interestingly, chronic infections that had been developed by using two different virus strains triggered partly very different responses. For example, major differences in the activation of immune responses were discovered between these two models. This indicates that the viruses have different kinds of abilities to manipulate the cellular defence systems," adds Hyöty.

Published in the iScience journal, the study revealed several mechanisms through which chronic enteroviral infections can impact pancreatic functioning and possibly the development of type 1 diabetes. The report is part of the ongoing doctoral studies of Doctoral Candidates Anni Honkimaa from Tampere University and Karoliina Hirvonen from the University of Turku.


Story Source:

Materials provided by University of Turku. Note: Content may be edited for style and length.


Journal Reference:

  1. Niina Lietzén, Karoliina Hirvonen, Anni Honkimaa, Tanja Buchacher, Jutta E. Laiho, Sami Oikarinen, Magdalena A. Mazur, Malin Flodström-Tullberg, Eric Dufour, Amir-Babak Sioofy-Khojine, Heikki Hyöty, Riitta Lahesmaa. Coxsackievirus B Persistence Modifies the Proteome and the Secretome of Pancreatic Ductal Cells. iScience, 2019; 19: 340 DOI: 10.1016/j.isci.2019.07.040

Cite This Page:

University of Turku. "Chronic enteroviral infection modifies broadly pancreatic cellular functions." ScienceDaily. ScienceDaily, 10 September 2019. <www.sciencedaily.com/releases/2019/09/190910105357.htm>.
University of Turku. (2019, September 10). Chronic enteroviral infection modifies broadly pancreatic cellular functions. ScienceDaily. Retrieved April 23, 2024 from www.sciencedaily.com/releases/2019/09/190910105357.htm
University of Turku. "Chronic enteroviral infection modifies broadly pancreatic cellular functions." ScienceDaily. www.sciencedaily.com/releases/2019/09/190910105357.htm (accessed April 23, 2024).

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