Sterile Neuroinflammation and Strategies for Therapeutic Intervention

Table 1

A putative list of DAMPs.

DAMPs	Neurological conditions	DAMPs releasing cells	Target cells	Target receptors	Downstream expression	References
HMGB1	Brain ischemia, TBI, stroke, ethanol exposure, AD, PD, HD	Injured neurons, oligodendrocyte-like cells, glial cells	Microglia, astrocytes, blood vessel-associated cells	RAGE, TLR2, TLR4	IL-1β, IFNγ, IL-1α, TNFα, IL-6	[20, 40, 88, 89, 92–94]
HSPs	TBI, stroke	Injured cells	Microglia	TLR2, TLR4, RAGE	TNFα, IL-1β, ICAM-1, VCAM-1, E-selection, iNOS	[105–107, 203]
S100B	AD, PD, HD	Astrocytes	Astrocytes, microglia	RAGE	Bcl-2 (antiapoptotic)	[112, 113]
DNA	Aging, TBI	Damaged or dead neurons	Astrocytes, microglia	TLR9	TNFα, IL-1β, RANTES	[125–129]
ATP	Stroke, PD, seizure	Damaged mitochondria	Microglia	NLRP3, P2X7RRAGE	TNFα, IL-6, COX-2, IL-8	[30, 131–133, 135, 136]

HMGB1, high mobility group box 1 protein; HSPs, heat shock proteins; S100B, calcium-modulated proteins B; DNA, deoxyribonucleic acid; ATP, adenosine triphosphate; TBI, traumatic brain injury; AD, Alzheimer’s disease; PD, Parkinson’s disease; HD, Huntington’s disease; RAGE, receptor for advanced glycation end products; TLR, toll-like receptor; IL, interleukin; TNF, tumor necrosis factors; IFN, interferon; ICAM, intercellular adhesion molecule; VCAM, vascular cell adhesion molecule; iNOS, inducible nitric oxide synthase; Bcl-2, b-cell lymphoma 2; RANTES, regulated on activation, normal T-cell expressed and secreted; COX-2, cyclooxygenase-2.