Inhibition of inflammation and hyperalgesia in NK-1 receptor knock-out mice.
We sought to characterise the contribution of the neuropeptide substance P to the outcome of two models of footpad inflammation of differing severity. In an intense inflammatory model produced by intra-plantar Mycobacterium tuberculosus (10 mg/ml) substantial reductions in footpad swelling, histological outcome and mechanical hyperalgesia were observed from early time points in mice lacking the neurokin-1 receptor for substance P compared with wild-type controls. Conversely, in a less intense model (M. tuberculosus 1 mg/ml) no differences were observed other than for a reduction in mechanical hyperalgesia at later time points (day 9 onwards). The results point to a previously unrecognised influence of substance P on peripheral tissue injury and the maintenance of hyperalgesia during more severe or more chronic phases of inflammatory disease.
Kidd
Bruce L
BL
Barts and the London School of Medicine, Queen Mary University of London, London, UK. b.l.kidd@qmul.ac.uk
Inglis
Julia J
JJ
Vetsika
Kelly
K
Hood
Vivienne C
VC
De Felipe
Carmen
C
Bester
Herve
H
Hunt
Stephen P
SP
Cruwys
Simon C
SC
D000818:Animals; D001169:Arthritis, Experimental / Q000139:chemically induced / Q000235:genetics* / Q000517:prevention & control; D005260:Female; D006930:Hyperalgesia / Q000235:genetics* / Q000517:prevention & control; D007249:Inflammation / Q000235:genetics* / Q000517:prevention & control; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D018040:Receptors, Neurokinin-1 / Q000172:deficiency* / Q000235:genetics*
D018040:Receptors, Neurokinin-1