Neuroinflammation

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Neuroinflammation, defined as an inflammatory reaction within nervous tissue, arises as a mechanism to protect the brain and spinal cord against potential harm from a variety of toxic stimuli including protein aggregates, neuronal injury, and infection. It is a complex response that involves activation of glial cells, secretion of inflammatory mediators, and production of reactive oxygen and nitrogen species. It is a highly controlled event that tends to be quickly resolved. However, continued exposure to a harmful stimulus can lead to chronic neuroinflammation, which is characterized by the persistent activation of glial cells, sustained release of inflammatory mediators, breakdown of the blood-brain barrier, and increased migration of peripheral immune cells into the central nervous system. These events establish a feedback loop that perpetuates and prolongs neuroinflammation. In recent years, research has shown that a sustained inflammatory response can contribute to the development and progression of many neurodegenerative diseases and neurological disorders.

R&D Systems offers an unparalleled selection of high-quality solutions for investigating all aspects of neuroinflammation.

Neuroinflammation Product Areas

CB₂ Receptors (CB2 R) CB₂ Receptor Agonists CB₂ Receptor Inverse Agonists CB₂ Receptor Modulators	ITK (ITK) ITK Inhibitors
Cell Adhesion Molecules Cell Adhesion Antagonists Cell Adhesion Inhibitors	Leukotriene and Related Receptors Leukotriene and Related Receptor Agonists Leukotriene and Related Receptor Inverse Agonists Leukotriene and Related Receptor Antagonists Additional Leukotriene and Related Products
Complement Complement Signaling Compounds	NFAT (View All) NFAT Inhibitors
Cyclooxygenases (COX-1, COX-2) Cyclooxygenase Inhibitors	Nitric Oxide Signaling Nitric Oxide Signaling Products
Cytokines and Receptors Cytokines and Growth Factors Cytokines and Receptors Research	Prostanoid Receptors Prostanoid Receptor Agonists Prostanoid Receptor Antagonists Additional Prostanoid Receptor Compounds
Gap Channels Gap Channel Blockers Gap Channel Controls	Purinergic (P2Y) Receptors Purinergic (P2Y) Receptor Agonists Purinergic (P2Y) Receptor Antagonists Purinergic (P2Y) Receptor Modulators Additional P2Y Receptor Compounds
Indoleamine 2,3 Dioxygenase (IDO) Indoleamine 2,3 Dioxygenase Inhibitors	RAGE (AGER) RAGE Antagonists
Inflammasomes Inflammasomes Agonists Inflammasomes Inhibitors Inflammasomes Activators	STING-Dependent Signaling (STING) STING-Dependent Signaling Agonists STING-Dependent Signaling Antagonists STING-Dependent Signaling Inhibitors STING-Dependent Signaling Degraders STING-Dependent Signaling Controls STING-dependent Signaling Compounds
IRAK (IRAK-1, IRAK-2, IRAK-3, IRAK-4) IRAK Inhibitors IRAK Degraders	Toll-like Receptors (View All) Toll-like Receptor Agonists Toll-like Receptor Antagonists Toll-like Receptor Inhibitors Toll-like Receptor Ligands Additional Toll-like Receptor Products

Background

The CNS is immune privileged, in that the blood brain barrier (BBB) protects it against peripheral circulating antibodies and the infiltration of peripheral immune cells. Immune response and inflammation in the CNS are regulated by microglial cells and their communication with other cell types, with the resulting processes being helpful and/or harmful.

Microglia are the key effector cells of neuroinflammation and are constantly surveying the cerebral environment to detect even the smallest pathogenic change. These cells belong to the myeloid cell lineage and enter the CNS during early embryonic development, with physiological roles in CNS development and mature synapse pruning. Microglia act as 'scavengers' in the CNS, removing damaged/apoptotic cells and protein plaques and tangles, through phagocytosis mediated by the complement system. Additionally, microglia communicate with and influence other CNS cells including astrocytes and neurons, releasing chemokines as well pro- and anti-inflammatory cytokines. The release of anti-inflammatory cytokines, as well as their ability to recruit neurons and astrocytes to sites of tissue damage allow microglia to promote tissue repair following neuroinflammation. However, microglia can also cause neurodegeneration through the production of proinflammatory cytokines and other cytotoxic substances to induce neuronal cell death.

There are no resident antigen presenting cells within the CNS, however when activated in response to tissue damage or injury, microglia can act as antigen presenting cells. When the BBB is compromised, peripheral circulating T-cells can cross the BBB and become activated by microglia that are presenting antigens. The production of antibodies against CNS proteins by infiltrating peripheral immune cells leads to autoimmune neurological disorders such as myasthenia gravis (MG). Inflammation resulting from damage to the BBB and infiltration of peripheral T-cells is also a pathogenic feature of multiple sclerosis (MS) and causes demyelination.

Neuroinflammation and immune response have been identified in neurodegenerative disorders, where they are a key pathogenic feature leading to cell death in Alzheimer's disease, amylotrophic lateral sclerosis, Parkinson's disease and MS or the primary cause of disease as in MG. Additionally neuroinflammation has also been identified as a feature of multiple neurological disorders such as depression and schizophrenia.