Jackb23
Senior Member
- Messages
- 293
- Location
- Columbus, Ohio
The study isn't particularly new but it is not old either. I know that miRNA-155 has been touched on within this website before and I believe this study to also be pertinent to ME/CFS.
MicroRNA 155 and viral-induced neuroinflammation
Laura L. Dickey, Timothy M. Hanley, Thomas B. Huffaker, Andrew G. Ramstead, Ryan M. O'Connell, Thomas E. Lane
"
Alejandro et al. (Lopez-Ramirez et al., 2014) discovered that miR-155 is upregulated in neurovascular units in active MS lesions compared to normal-appearing white matter in MS patients. In addi- tion, the group used the EAE model to show that miR-155 expression is dramatically increased in mice with hind-limb paralysis during the recovery phase, and that miR-155 regulates blood-brain-barrier (BBB) function. The latter finding is consistent with a study byLopez-Ramirezet al. (2014) showing that miR-155 negatively regulates blood-brain-barrier permeability by targeting the cell-cell complex mol- ecules annexin-2 and claudin1, as well as the adhesion components DOCK-1 and syntenin-1."
"Not surprisingly, multiple reports identify miR-155 as important in mediating host responses to microbial diseases (Zeng et al., 2015), in- cluding viral infections with members of the Herpesviridae,Coronaviridae, Arenaviridae, Flaviviridae, and Retroviridae families (discussed further below) (Yao and Nair, 2014; Kaluzna, 2014; Gottwein, 2013; Bhela et al., 2015; Bhela et al., 2014; Dickey et al., 2016; Dudda et al., 2013; Lind et al., 2013; Lu et al., 2011; Martinez-Nunez et al., 2009; Napuri et al., 2013; Zawislak et al., 2013). Recently, miR-155 has been shown to tailor immune responses in models of viral-induced neurologic disease, and numerous mechanisms by which miR-155 controls immune responses following viral infection have been identified. For example, multiple studies have demonstrated that T cell responses are impaired in the absence of miR-155 during in- fection with certain neurotropic viruses (Lu et al., 2015; Bhela et al., 2015; Bhela et al., 2014; Dickey et al., 2016; Dudda et al., 2013; Lind et al., 2013; Zawislak et al., 2013)."
Mechanisms of miR-155-mediated regulation of neuroinflammation:
Herpes simplex virus:
Modulates disease severity and viral load in CNS Regulates accumulation of CD8+ T cells
Affects number of CD8+ T cells that produce TNF-αand/or IFN-γ
Necessary for optimal expression of homing molecules VLA-4 and CD44
Important for Th1 and Th17 cell accumulation in lymph nodes and spleens
Promotes CD4+ T cell proliferation
Regulates expression of IL-1β, IL-6, IFN-γ, and IL-16 Regulates levels of SHIP1 and IFN-γRα in activated CD4+ T cells
Cytomegalovirus:
Critical for expansion of effector NK cells
Regulates survival of NK cells
Necessary for optimal memory NK cell generation Targets Noxa and SOCS1
Lymphocytic choriomeningitis virus:
Necessary for optimal CD4+ and CD8+ T cell responses Necessary for optimal CD8+ T cell proliferation Necessary for optimal CD8+ T cell survival by interfering with PI3/Akt pathway
Regulates cytokine signaling by targeting SOCS1
Targets SOCS1 to regulate expansion of virus-specific NK cells
Targets SOCS1 to regulate maintenance of virus-specific CD8+ T cells during chronic infection
Japanese encephalitis virus:
Mediates disease severity
Regulates expression of IFN-β, TNF-α, IL-10, MCP-1, IL-6, IRF-3/7, IRF-8, CFH, and TBK-1
Negatively regulates SHIP1 expression
Contributes to JEV-induced microglial activation and neuronal death"
http://labs.path.utah.edu/oconnell/publications/28139244.pdf
MicroRNA 155 and viral-induced neuroinflammation
Laura L. Dickey, Timothy M. Hanley, Thomas B. Huffaker, Andrew G. Ramstead, Ryan M. O'Connell, Thomas E. Lane
"
Alejandro et al. (Lopez-Ramirez et al., 2014) discovered that miR-155 is upregulated in neurovascular units in active MS lesions compared to normal-appearing white matter in MS patients. In addi- tion, the group used the EAE model to show that miR-155 expression is dramatically increased in mice with hind-limb paralysis during the recovery phase, and that miR-155 regulates blood-brain-barrier (BBB) function. The latter finding is consistent with a study byLopez-Ramirezet al. (2014) showing that miR-155 negatively regulates blood-brain-barrier permeability by targeting the cell-cell complex mol- ecules annexin-2 and claudin1, as well as the adhesion components DOCK-1 and syntenin-1."
"Not surprisingly, multiple reports identify miR-155 as important in mediating host responses to microbial diseases (Zeng et al., 2015), in- cluding viral infections with members of the Herpesviridae,Coronaviridae, Arenaviridae, Flaviviridae, and Retroviridae families (discussed further below) (Yao and Nair, 2014; Kaluzna, 2014; Gottwein, 2013; Bhela et al., 2015; Bhela et al., 2014; Dickey et al., 2016; Dudda et al., 2013; Lind et al., 2013; Lu et al., 2011; Martinez-Nunez et al., 2009; Napuri et al., 2013; Zawislak et al., 2013). Recently, miR-155 has been shown to tailor immune responses in models of viral-induced neurologic disease, and numerous mechanisms by which miR-155 controls immune responses following viral infection have been identified. For example, multiple studies have demonstrated that T cell responses are impaired in the absence of miR-155 during in- fection with certain neurotropic viruses (Lu et al., 2015; Bhela et al., 2015; Bhela et al., 2014; Dickey et al., 2016; Dudda et al., 2013; Lind et al., 2013; Zawislak et al., 2013)."
Mechanisms of miR-155-mediated regulation of neuroinflammation:
Herpes simplex virus:
Modulates disease severity and viral load in CNS Regulates accumulation of CD8+ T cells
Affects number of CD8+ T cells that produce TNF-αand/or IFN-γ
Necessary for optimal expression of homing molecules VLA-4 and CD44
Important for Th1 and Th17 cell accumulation in lymph nodes and spleens
Promotes CD4+ T cell proliferation
Regulates expression of IL-1β, IL-6, IFN-γ, and IL-16 Regulates levels of SHIP1 and IFN-γRα in activated CD4+ T cells
Cytomegalovirus:
Critical for expansion of effector NK cells
Regulates survival of NK cells
Necessary for optimal memory NK cell generation Targets Noxa and SOCS1
Lymphocytic choriomeningitis virus:
Necessary for optimal CD4+ and CD8+ T cell responses Necessary for optimal CD8+ T cell proliferation Necessary for optimal CD8+ T cell survival by interfering with PI3/Akt pathway
Regulates cytokine signaling by targeting SOCS1
Targets SOCS1 to regulate expansion of virus-specific NK cells
Targets SOCS1 to regulate maintenance of virus-specific CD8+ T cells during chronic infection
Japanese encephalitis virus:
Mediates disease severity
Regulates expression of IFN-β, TNF-α, IL-10, MCP-1, IL-6, IRF-3/7, IRF-8, CFH, and TBK-1
Negatively regulates SHIP1 expression
Contributes to JEV-induced microglial activation and neuronal death"
http://labs.path.utah.edu/oconnell/publications/28139244.pdf