Anti-inflammatory genes in PBMCs post-spontaneous intracerebral hemorrhage

Abstract

Background Neuroinflammation is important in the pathophysiology of spontaneous intracerebral hemorrhage (ICH) and peripheral inflammatory cells play a role in the clinical evolution and outcome. Methodology Blood samples from ICH patients (n = 20) were collected at admission for 5 consecutive days for peripheral blood mononuclear cells (PBMCs). Frozen PBMCs were used for real-time PCR using Taqman probes (NFKB1, SOD1, PPARG, IL10, NFE2L2, and REL) and normalized to GAPDH. Data on hospital length of stay and modified Rankin score (MRS) were collected with 90-day MRS ≤ 3 as favorable outcome. Statistical analysis of clinical characteristics to temporal gene expression from early to delayed timepoints was compared for MRS groups (favorable vs unfavorable) and hematoma volume. Principle findings and results IL10, SOD1, and REL expression were significantly higher at delayed timepoints in PBMCs of ICH patients with favorable outcome. PPARG and REL increased between timepoints in patients with favorable outcome. NFKB1 expression was not sustained, but significantly decreased from higher levels at early onset in patients with unfavorable outcome. IL10 expression showed a negative correlation in patients with high hematoma volume (>30 mL). Conclusions and significance Anti-inflammatory, pro-survival regulators were highly expressed at delayed time points in ICH patients with a favorable outcome, and IL10 expression showed a negative correlation to high hematoma volume.

Efficacy and Safety of Endoscopic Surgery Versus Craniotomy for Hypertensive Putamen Hemorrhage

“…This inflammatory response encompasses a series of inflammatory cells, including leukocytes, macrophages, microglia, and astrocytes, alongside a range of inflammatory mediators such as matrix metalloproteinases, nuclear factor erythroid 2-related factor 2 (NRF2), heme oxygenase, iron, and interleukin-10 (IL-10). [18][19][20][21] An alternative hypothesis posits that thrombin-induced autophagy within the cerebral environment plays a crucial role, 22 with the neurotoxicity closely associated with the activation of NF-κB. 23 Numerous randomized controlled trials have shown no advantage of hemorrhage evacuation over conservative treatment, 3 except in the case of endoscopic surgery.…”

“…The prevailing conjecture suggests that neurotoxicity is associated with an inflammatory reaction triggered by the immune system’s activation in response to the hematoma. This inflammatory response encompasses a series of inflammatory cells, including leukocytes, macrophages, microglia, and astrocytes, alongside a range of inflammatory mediators such as matrix metalloproteinases, nuclear factor erythroid 2-related factor 2 (NRF2), heme oxygenase, iron, and interleukin-10 (IL-10) 18–21 . An alternative hypothesis posits that thrombin-induced autophagy within the cerebral environment plays a crucial role, 22 with the neurotoxicity closely associated with the activation of NF-κB 23 …”