DAMPening Inflammation by Modulating TLR Signalling

Table 1

DAMPs induce disease in vivo. Administration of DAMPs to rodents either intra-articularly (i.a.), intracerebroventricularly (i.c.), intraperitoneally (i.p.), intratracheally (i.t.), or intravenously (i.v.) can provoke pathological inflammation in vivo.

Pathology	DAMP	Effect	Refs
Atherosclerosis	Apo CIII-rich VLDL (i.v.)	Stimulated TLR2 dependent monocyte activation and adhesion	[128]
Brain injury	HMGB1 (i.c.)	Increased cytokines, taste aversion, fever, mechanical allodynia, promotes severity of infarction	[129–131]
Gut inflammation	HMGB1 (B box) (i.p.)	Increased ileal mucosal permeability and bacterial translocation to mesenteric lymph nodes	[132]
Joint disease	FNEDA (i.a.)	Induced TLR4 dependent transient ankle swelling, cytokine synthesis, synovial inflammation	[86]
	HMGB1 (i.a.)	Induced synovial inflammation, some pannus formation	[133]
	Tenascin-C (i.a.)	Induced TLR4 dependent joint inflammation and tissue erosion	[24]
Liver injury	DNA	During acetaminophen induced cell death induced TLR9 dependent tissue injury	[134]
	HMGB-1 (i.p.)	Aggravated ischemic reperfusion injury	[135]
Lung injury	HMGB-1 (i.t.)	Stimulated acute inflammatory injury, neutrophil accumulation, edema, cytokine production	[136–138]
Sepsis	HS (i.p.)	Induced TLR4 dependent lethality	[121]
	HMGB1 (i.p.)	Induced partially TLR4 dependent lethality	[114]