• Can changes in EEG improve neuropathic pain treatments - read Nov newsletter.
  • Nine posters ready to reveal at the SfN virtual conference 8-11 Nov, booth 1818.
  • Joined-up preclinical and clinical trials to advance psilocybin drug development
  • Transpharmation joins HaPpY team to help break the vicious cycle of chronic pain & mood disorders, see News for details
  • Announcing new premises in Poland with a focus on neuropsychiatric disorders...
  • New state-of-the-art premises at Discovery Park, Kent

Inflammation / Neuroinflammation

The anti-inflammatory therapeutics market is expected to be valued at 130.6 billion USD by 2026, reflecting the demand for effective novel therapeutics for inflammatory disorders, which constitutes significant global disease burden.

Inflammation is typically an acute response of the body’s immune system to infection or damage, but when this immune response becomes dysregulated, chronic inflammation can cause more harm than good. Inflammation in the periphery is mediated largely by peripheral blood mononuclear cells in disorders such as cancers, autoimmune disorders and metabolic disorders. In the CNS, the brain-resident macrophages known as microglia mediate the immune response in neurodegenerative disorders such as Alzheimer’s Parkinson’s and Multiple Sclerosis. It is well established that inflammation is a key driver of these degenerative diseases.

Both in vitro and in vivo models of inflammation are commonly used to characterise the inflammatory response to pro-inflammatory stimuli such as lipopolysaccharide (LPS) and adenosine triphosphate (ATP), providing a platform on which to test the efficacy of novel anti-inflammatory therapeutics.

Examples of the models we offer:

  • PBMCs: LPS-induced inflammation in rodent and human cells
  • Whole Blood: LPS-induced inflammation in rodent and human samples
  • NLRP3-mediated inflammation: LPS and ATP-induced IL-1Beta release in human whole blood
  • LPS and cytokine induced systemic inflammation in rodents
  • LPS and cytokine induced neuroinflammation in rodents
  • Clinical sample procurement and analysis

Examples of end points:

  • Analysis of cytokines and chemokines in fluids and tissue
  • Immunohistochemistry
  • Measure activation of intracellular signalling pathways by infrared western blotting
  • In vivo physiological measurements  (e.g., body temperature)

pain1This list is not exhaustive, we are always developing new areas of discovery within our preclinical field of expertise. If there is something particular that is not listed here please do contact us.

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