Salmonella Typhimurium infection: Type I Interferons integrate cellular networks to disintegrate macrophages
Authors:Nirmal Robinson1,2
1 Cluster of Excellence in Cellular Stress Responses in Aging-associated Diseases (CECAD), University of Cologne, Cologne, Germany.
2 Institute for Medical Microbiology, Immunology and Hygiene, University Hospital Cologne, Cologne, Germany.
Keywords:
Salmonella, interferon, Nrf2, RIP, p62, PGAM5, macrophage, autophagy, cell death, necroptosis.
Corresponding Author(s):
Conflict of interest statement:
The author states that he has no conflict of interest.
Please cite this article as:
Nirmal Robinson (2018). Salmonella Typhimurium infection: Type I Interferons integrate cellular networks to disintegrate macrophages. Cell Stress 2(2): 37-39. doi: 10.15698/cst2018.02.125
© 2018 Robinson. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
Type I interferons have immunomodulatory functions during infection with bacteria and viruses. They are vital for the host defense against viruses and extracellular bacteria. However, recent evidences show that IFN-I contributes to immunopathology during intracellular bacterial infection. We had previously shown that IFN-I receptor knock out mice (ifnar-/-) are less susceptible to S. Typhimurium infection and the macrophages are resistant to S. Typhimurium-induced cell death dependent on RIP kinases commonly known as necroptosis. We have now recently shown that IFN-I-signaling through the activation of RIP kinases and PGAM5 exacerbates necroptosis in Salmonella Typhimurium-infected macrophages by downregulating Nrf2-dependent cytoprotective response mechanisms [Hos et al, JCB 2017].