tetano
Editor, Senior Moderator
Virology
. 2021 Dec 2;566:122-135.
doi: 10.1016/j.virol.2021.11.012. Online ahead of print.
Matrix metalloproteinases and tissue inhibitors of metalloproteinases in murine β-coronavirus-induced neuroinflammation
Sourodip Sengupta[SUP] 1 [/SUP], Sankar Addya[SUP] 2 [/SUP], Diptomit Biswas[SUP] 1 [/SUP], Paromita Banerjee[SUP] 1 [/SUP], Jayasri Das Sarma[SUP] 3 [/SUP]
Affiliations
Abstract
Mouse hepatitis virus (MHV; m-β-CoV) serves as a useful model for studying the cellular factors involved in neuroinflammation. To understand the role of matrix metalloproteinases (MMPs) in neuroinflammation, brain tissues from m-β-CoV-infected mice were harvested at different days post-infection (d.p.i) and investigated for Mmp expression by RT-qPCR. Mmp-2, -3, -8, -12 showed significant mRNA upregulation peaking with viral replication between 5 and 6 d.p.i. Elevated levels of MMP regulator TIMP-1 are suggestive of a TIMP-1 mediated host antiviral response. Biological network assessment suggested a direct involvement of MMP-3, -8, -14 in facilitating peripheral leukocyte infiltrations. Flow cytometry confirmed the increased presence of NK cells, CD4[SUP]+[/SUP] and CD8[SUP]+[/SUP] T cells, neutrophils, and MHCII expressing cells in the m-β-CoV infected mice brain. Our study revealed that m-β-CoV upregulated Park7, RelA, Nrf2, and Hmox1 transcripts involved in ROS production and antioxidant pathways, describing the possible nexus between oxidative pathways, MMPs, and TIMP in m-β-CoV-induced neuroinflammation.
Keywords: MHV-A59; MMPs; Neuroinflammation; ROS; TIMPs; β-coronavirus (β-CoV).
. 2021 Dec 2;566:122-135.
doi: 10.1016/j.virol.2021.11.012. Online ahead of print.
Matrix metalloproteinases and tissue inhibitors of metalloproteinases in murine β-coronavirus-induced neuroinflammation
Sourodip Sengupta[SUP] 1 [/SUP], Sankar Addya[SUP] 2 [/SUP], Diptomit Biswas[SUP] 1 [/SUP], Paromita Banerjee[SUP] 1 [/SUP], Jayasri Das Sarma[SUP] 3 [/SUP]
Affiliations
- PMID: 34906793
- DOI: 10.1016/j.virol.2021.11.012
Abstract
Mouse hepatitis virus (MHV; m-β-CoV) serves as a useful model for studying the cellular factors involved in neuroinflammation. To understand the role of matrix metalloproteinases (MMPs) in neuroinflammation, brain tissues from m-β-CoV-infected mice were harvested at different days post-infection (d.p.i) and investigated for Mmp expression by RT-qPCR. Mmp-2, -3, -8, -12 showed significant mRNA upregulation peaking with viral replication between 5 and 6 d.p.i. Elevated levels of MMP regulator TIMP-1 are suggestive of a TIMP-1 mediated host antiviral response. Biological network assessment suggested a direct involvement of MMP-3, -8, -14 in facilitating peripheral leukocyte infiltrations. Flow cytometry confirmed the increased presence of NK cells, CD4[SUP]+[/SUP] and CD8[SUP]+[/SUP] T cells, neutrophils, and MHCII expressing cells in the m-β-CoV infected mice brain. Our study revealed that m-β-CoV upregulated Park7, RelA, Nrf2, and Hmox1 transcripts involved in ROS production and antioxidant pathways, describing the possible nexus between oxidative pathways, MMPs, and TIMP in m-β-CoV-induced neuroinflammation.
Keywords: MHV-A59; MMPs; Neuroinflammation; ROS; TIMPs; β-coronavirus (β-CoV).