Injection of lentiviral miR-126-5p improved behavioral outcomes at 3 days after stroke (<i>P</i><0.05). miR-126-3p and -5p overexpression downregulated the expression of proinflammatory cytokines IL-1β and TNF-α and adhesion molecules VCAM-1 and E-selectin, as well as decreased MPO<sup>+</sup> (myeloperoxidase positive) cell numbers at 3 days after ischemia (<i>P</i><0.05).
Interleukin-1β is a potent proinflammatory cytokine that plays a key role in the pathogenesis of the brain aging and diverse range of neurological diseases including Alzheimer's disease, Parkinson's disease, stroke and persistent pain.
In both a murine model of stroke and in patients, increased IL-1β levels were observed after stroke, and hypothermia treatment was associated with lower IL-1β levels.
Interleukin(IL)-37 is an immunosuppressive cytokine belonging to the IL-1 superfamily with no mouse homologue yet identified, the effects of which have not been studied in stroke.
The objective of the study is to assess the modulatory effect of IL-1 genotypes on risk mediated by Lp(a) METHODS: We assessed whether IL-1 genotypes modulate the effect of Lp(a) on major adverse cardiovascular events (cardiovascular death, myocardial infarction, and stroke/transient ischemic attack) and angiographically determined coronary artery disease (CAD).
After adjusting for stroke severity and infections, higher ex vivo TNFα (OR 0.29, 95%CI 0.11-0.72, P = 0.01), IP-10 (OR 0.25, 95%CI 0.08-0.73, P = 0.01), IL-1β (OR 0.42, 95%CI 0.20-0.89, P = 0.02), and IL-12 (OR 0.07, 95%CI 0.01-0.70, P = 0.02) release was associated with the reduced risk of delirium.
These data provide evidence that serum TNF-α and IL-1β concentrations are related to poor long-term outcomes after stroke in the presence of particular alleles.
Intracellular levels of TNF-α and IL-1β in microglia peaked at 3 days of stroke, and IL-4<sup>+</sup> IL-10<sup>+</sup> double-positive microglia significantly increased at day 10.
This work was designed to examine the effect of mouse recombinant resistin on mRNA expression of Tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-10 (IL-10), Transforming growth factor-β1 (TGF- β1), and Heat shock protein-70 (HSP-70) in mouse model of stroke.
Given the established role of IL-1β in stroke, we tested the efficacy of the murine Canakinumab-equivalent antibody in a mouse model of ischaemic stroke.
Stroke significantly increases macrophage infiltration into the heart and increases IL-1β, IL-6, MCP-1, TGF-β and macrophage-associated inflammatory cytokine levels in the heart as well as induces cardiac-fibrosis and hypertrophy.
Quantitative PCR analysis of whole cell lysate as well as flow-sorted myeloid cells from the perilesional cortex showed increased cellular interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α) mRNA levels but reduced plasma levels of these cytokines in MS P2X4R KO mice after stroke.
These findings indicate the important roles that TNF-α and IL-1β serum levels play regarding the risk of PSD, particularly during the acute phase of stroke and in patients with genetic susceptibility.
MAPC treatment restored spleen mass reduction caused by stroke, elevated Treg cells within the spleen, increased IL-10 and decreased IL-1β released by splenocytes.
Subjects carrying the TT genotype of the -511C/TIL-1beta polymorphism showed a decreased risk of MI (odds ratio [OR], 0.36; 95% CI, 0.20 to 0.64) and stroke (OR, 0.32; 95% CI, 0.13 to 0.81) after adjustment for conventional risk factors.
Subjects carrying the TT genotype of the -511C/T IL-1beta polymorphism showed a decreased risk of MI (odds ratio [OR], 0.36; 95% CI, 0.20 to 0.64) and stroke (OR, 0.32; 95% CI, 0.13 to 0.81) after adjustment for conventional risk factors.
IL-1 mediates host defence responses to local and systemic disease and injury (e.g. fever, slow-wave sleep, appetite suppression and neuroendocrine responses) and to neuroinflammation and cell death in neurodegenerative conditions, such as stroke and head injury.