Peripheral blood immune cells from individuals with Parkinson's disease or inflammatory bowel disease share deficits in iron storage and transport that are modulated by non-steroidal anti-inflammatory drugs

Neurobiology of Disease, Journal Year: 2025, Volume and Issue: unknown, P. 106794 - 106794

Published: Jan. 1, 2025

Parkinson's Disease (PD) is a multisystem disorder in which dysregulated neuroimmune crosstalk and inflammatory relay via the gut-blood-brain axis have been implicated PD pathogenesis. Although alterations circulating cytokines reactive oxygen species (ROS) associated with PD, no biomarkers identified that predict clinical progression or disease outcome. Gastrointestinal (GI) dysfunction, involves perturbation of underlying immune system, an early often-overlooked symptom affects up to 80 % individuals living PD. Interestingly, 50-70 bowel (IBD), GI condition has epidemiologically linked display chronic illness-induced anemia - drives toxic accumulation iron gut. Ferroptotic (or loaded) cells small dysmorphic mitochondria-suggesting mitochondrial dysfunction consequence accumulation. In pro-inflammatory environments, accumulates cells, suggesting possible connection and/or synergy between dysregulation cell dysfunction. Peripheral blood mononuclear (PBMCs) recapitulate certain PD-associated neuropathological signatures can act as communicating messengers gut-brain axis. Additionally, this communication be modulated by several environmental factors; specifically, our data further support existing literature demonstrating role for non-steroidal anti-inflammatory drugs (NSAIDs) modulating transcriptional states inflamed individuals. A mechanism linking gut inflammation function within peripheral yet conferring risk To end, we isolated PBMCs simultaneously evaluated their directed transcriptome bioenergetic status, investigate if sensitization are IBD because remittent activation. We shared features immunometabolism may contribute epidemiological association reported

Language: Английский

IL-6 and diabetic kidney disease

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Dec. 19, 2024

Diabetic kidney disease (DKD) is a severe microvascular complication of diabetes associated with high mortality and disability rates. Inflammation has emerged as key pathological mechanism in DKD, prompting interest novel therapeutic approaches targeting inflammatory pathways. Interleukin-6 (IL-6), well-established cytokine known for mediating various responses, attracted great attention the DKD field. Although multiple

Language: Английский

Peripheral Blood Immune Cells from Individuals with Parkinson's Disease or Inflammatory Bowel Disease Share Deficits in Iron Storage and Transport that are Modulated by Non-Steroidal Anti-Inflammatory Drugs

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Aug. 19, 2024

ABSTRACT Parkinson’s Disease (PD) is a multisystem disorder in which dysregulated neuroimmune crosstalk and inflammatory relay via the gut-blood-brain axis have been implicated PD pathogenesis. Although alterations circulating cytokines reactive oxygen species (ROS) associated with PD, no biomarkers identified that predict clinical progression or disease outcome. Gastrointestinal (GI) dysfunction, involves perturbation of underlying immune system, an early often-overlooked symptom affects up to 80% individuals living PD. Interestingly, 50-70% bowel (IBD), GI condition has epidemiologically linked display chronic illness-induced anemia — drives toxic accumulation iron gut. Ferroptotic (or loaded) cells small dysmorphic mitochondria—suggesting mitochondrial dysfunction consequence accumulation. In pro-inflammatory environments, accumulates cells, suggesting possible connection and/or synergy between dysregulation cell dysfunction. Peripheral blood mononuclear (PBMCs) recapitulate certain PD-associated neuropathological signatures can act as communicating messengers gut-brain axis. Additionally, this communication be modulated by several environmental factors; specifically, our data further support existing literature demonstrating role for non-steroidal anti-inflammatory drugs (NSAIDs) modulating transcriptional states inflamed individuals. A mechanism linking gut inflammation function within peripheral yet conferring risk To end, we isolated PBMCs simultaneously evaluated their directed transcriptome bioenergetic status, investigate if sensitization are IBD because remittent activation. We shared features immunometabolism may contribute epidemiological association reported

Language: Английский