Table 2

Key concepts and their relations to CRPS and NFκB
Key concept	Relation to CRPS	Relation to NFκB

Substance P	Locally elevated upon electrical C-fiber stimulation [16, 98]	Induces NFκB mediated release of IL-6 and TNFα [103]
Calcitonin Gene-related Protein	Systemically and locally elevated [13, 16, 98]	Suppresses NFκB activity in thymic cells [104]
Bradykinin	Systemically elevated [13]	Activates NFκB [46, 51]
Vasoactive Intestinal Protein	Systemically elevated [13] Locally decreased [99]	Inhibits NFκB mediated chemokine production by macrophages [52]. Prevents NFκB binding to promoter site for NO [52]
Neuropeptide Y	Systemically elevated [13]	NPY-Y1-R expression is regulated by NFκB [54]
Neutral Endopeptidase	Speculated to be decreased [19]	No relation with NFκB described
Angiotensin Converting Enzyme	Speculated to be decreased [19] Polymorphism in CRPS patients [79]	Reduces NFκB activity [55]
TNFα	Locally increased [10]	Induced by NFκB [48], Activates NFκB [100]
IL-1β	Locally increased [10]	Stimulates NFκB mediated apoptosis in sympathetic neurons [101]
IL-6	Locally increased [10]	Induced by NFκB [49]
Tryptase	Locally increased [10]	Induced by NFκB [103]
Free radicals	Signs of free radical damage [24]	Second messenger in NFκB activity [50, 59]
Nitric oxide	Elevated after monocyte stimulation [102]	NO reduces NFκB activity, but ONOO induces NFκB [45, 56, 57]
Protons (acidosis)	Lactate increased in skin [20]	Influences NFκB activity [22, 61, 62]
α-receptor	Up-regulated in analgesic skin ([72]	Pro-inflammatory responses mediated through NFκB [68-70]
Sympathetic neuron	Speculated to be damaged in CRPS [105]	NFκB mediates Il-1βinduced apoptosis [101]
NMDA receptor	Role in development of central sensitization [28].	NFκB is involved in the up-regulation of some types of NMDA receptors [63].

Hettne et al. Journal of Biomedical Discovery and Collaboration 2007 2:2 doi:10.1186/1747-5333-2-2