Here, we show in wild-type (WT) experimental autoimmune encephalomyelitis (EAE) mice that PGC-1α is decreased 13 d after EAE induction followed by a steady decline up to 20 d. These changes were accompanied by parallel alterations in levels of superoxide dismutase 2, peroxiredoxin 3, thioredoxin 2, UCP4, and UCP5.
Here, we show in wild-type (WT) experimental autoimmune encephalomyelitis (EAE) mice that PGC-1α is decreased 13 d after EAE induction followed by a steady decline up to 20 d. These changes were accompanied by parallel alterations in levels of superoxide dismutase 2, peroxiredoxin 3, thioredoxin 2, UCP4, and UCP5.
Here, we show in wild-type (WT) experimental autoimmune encephalomyelitis (EAE) mice that PGC-1α is decreased 13 d after EAE induction followed by a steady decline up to 20 d. These changes were accompanied by parallel alterations in levels of superoxide dismutase 2, peroxiredoxin 3, thioredoxin 2, UCP4, and UCP5.
Effective IFN-β therapy in B cell-independent EAE was associated with reduced inflammatory T cells in the CNS and skewed splenic B cells towards an immature population and away from a germinal center population.
Our results revealed that the serum concentrations of T-helper 1 (Th1) and Th17 cytokines, interleukin (IL)-6, IL-1β, IL-1α and prostaglandin E2 in EAE mice were significantly higher than controls.
Our results revealed that the serum concentrations of T-helper 1 (Th1) and Th17 cytokines, interleukin (IL)-6, IL-1β, IL-1α and prostaglandin E2 in EAE mice were significantly higher than controls.
The increased amounts of the i-20S-specific subunit β5i and PA28α/β in EAE correlate with the levels of interferon-γ and its downstream effectors p-signal transducer and activator of transcription 1 and interferon regulatory factor-1, but not with those of nuclear factor kappa-light-chain-enhancer of activated B cells.
The increased amounts of the i-20S-specific subunit β5i and PA28α/β in EAE correlate with the levels of interferon-γ and its downstream effectors p-signal transducer and activator of transcription 1 and interferon regulatory factor-1, but not with those of nuclear factor kappa-light-chain-enhancer of activated B cells.
Together, these findings suggest that a combination of subunit displacement and reduced Nrf1 expression may be responsible for c-20S impairment in EAE.
Decreased levels of constitutive proteasomes in experimental autoimmune encephalomyelitis may be caused by a combination of subunit displacement and reduced Nfe2l1 expression.
Interleukin-1β (IL-1β), tumor necrosis factor α (TNFα), and IL-6 expression were robustly increased in the DH of mice with EAE manifesting pain, whereas these cytokines showed a modest increase or no change in mice with EAE in the absence of pain.
Interleukin-1β (IL-1β), tumor necrosis factor α (TNFα), and IL-6 expression were robustly increased in the DH of mice with EAE manifesting pain, whereas these cytokines showed a modest increase or no change in mice with EAE in the absence of pain.
Interleukin-1β (IL-1β), tumor necrosis factor α (TNFα), and IL-6 expression were robustly increased in the DH of mice with EAE manifesting pain, whereas these cytokines showed a modest increase or no change in mice with EAE in the absence of pain.
The present studies investigated the role of PMCA2 in neuropathic pain processing in the DH of wild-type mice affected by experimental autoimmune encephalomyelitis (EAE), an animal model of MS, and following SCI.
The study suggests β-adrenoceptor-mediated neuroinflammation-promoting role of noradrenaline in EAE via modulation of microglial Nrf2 expression, and thereby forms the basis for further translational pharmacological research to improve multiple sclerosis therapy.
The study suggests β-adrenoceptor-mediated neuroinflammation-promoting role of noradrenaline in EAE via modulation of microglial Nrf2 expression, and thereby forms the basis for further translational pharmacological research to improve multiple sclerosis therapy.
We then monitored the thickness of the retinal layers in different EAE models: in wild-type (WT) C57Bl/6J mice immunized with myelin oligodendrocyte glycoprotein peptide (MOG<sub>35-55</sub>) or with bovine myelin basic protein (MBP), in TCR<sup>2D2</sup> mice immunized with MOG<sub>35-55</sub>, and in SJL/J mice immunized with myelin proteolipid lipoprotein (PLP<sub>139-151</sub>).
We then monitored the thickness of the retinal layers in different EAE models: in wild-type (WT) C57Bl/6J mice immunized with myelin oligodendrocyte glycoprotein peptide (MOG<sub>35-55</sub>) or with bovine myelin basic protein (MBP), in TCR<sup>2D2</sup> mice immunized with MOG<sub>35-55</sub>, and in SJL/J mice immunized with myelin proteolipid lipoprotein (PLP<sub>139-151</sub>).
<b>Results:</b><sup>89</sup>Zr-labeled anti-cd20 mAb was effectively absorbed from s.c. and i.v. injection sites and distributed to all major organs in the EAE and control mice.
<b>Results:</b><sup>89</sup>Zr-labeled anti-cd20 mAb was effectively absorbed from s.c. and i.v. injection sites and distributed to all major organs in the EAE and control mice.
Our results show that LFA-1 plays a pivotal role in T cell motility during EAE and suggest that interfering with the molecular mechanisms controlling T cell motility can help to reduce the pathogenic potential of autoreactive lymphocytes.
Our results show that LFA-1 plays a pivotal role in T cell motility during EAE and suggest that interfering with the molecular mechanisms controlling T cell motility can help to reduce the pathogenic potential of autoreactive lymphocytes.
Furthermore, there was a reduction in the levels of inflammatory cytokines including IL-17 (<i>P </i>= 0.009) and IL-23 (<i>P </i>= 0.012) and confirmed increased serum antioxidant levels in <i>A. dracunculus</i> treated EAE mice (<i>P </i>= 0.008).<b>Conclusions:</b> These observations indicate that <i>A. dracunculus</i> extracts could reduce inflammatory cytokines and attenuate certain signs of EAE, suggesting the potential of a useful adjuvant therapy for MS.
Furthermore, there was a reduction in the levels of inflammatory cytokines including IL-17 (<i>P </i>= 0.009) and IL-23 (<i>P </i>= 0.012) and confirmed increased serum antioxidant levels in <i>A. dracunculus</i> treated EAE mice (<i>P </i>= 0.008).<b>Conclusions:</b> These observations indicate that <i>A. dracunculus</i> extracts could reduce inflammatory cytokines and attenuate certain signs of EAE, suggesting the potential of a useful adjuvant therapy for MS.
This study demonstrates that E2 treatment induced three heightened regulatory mechanisms that potentially protect IL-10 KO mice from EAE: (1) an increase in programmed death-ligands 1 and 2 on monocytes and macrophages in the periphery and within the CNS; (2) an increase in CD73 in the inflamed CNS, which can increase the production of the anti-inflammatory molecule adenosine; and (3) a decrease in CD4<sup>+</sup>CD25<sup>+</sup>FoxP3<sup>+</sup> regulatory T cells in the spleen.