Author(s) : Riccardo ROSSI, Olle JOHANSSON, Experimental Dermatology Unit, Department of Neuroscience, Karolinska Institute, 171 77 Stockholm, Sweden..
Summary : Noxious stimuli may directly activate peripheral nerve endings of primary sensory neurons. Such impulses are conveyed centrally as well as, through antidromic axon-reflexes, peripherally where they release pro-inflammatory neuropeptides that cause the set of changes collectively referred to as “neurogenic inflammation”. These peptides are able to regulate cutaneous inflammatory processes. Thus, for instance, quantitative variations in cutaneous levels of some neuropeptides, such as calcitonin gene-related peptide, neuropeptide Y, substance P, vasoactive intestinal polypeptide, neurokinin A and somatostatin, have been found in lesional skin in a number of dermatoses. In addition, they may also serve as selective markers of nerve fiber degeneration and regeneration, and they can also act as trophic agents.
Figure 1. Confocal immunofluorescence image of a 90 µm-thick section
from human skin after incubation with antibodies to protein gene product
9.5 to reveal the entire peripheral innervation.
Figure 2. Schematic drawing of human skin indicating the large number
of peptides present.
Figure 3. A single epidermal nerve fiber seen in image processing mode
using peptide-based immunohistochemistry.
Figure 4. Methionine-enkephalin-containing cells in a human Merkel cell
tumour.
Figure 5. 3-D confocal image of a somatostatin-immunoreactive epidermal
Langerhans cell.
Figure 6. Colour-coded representation of a somatostatin-positive epidermal
Langerhans cell showing a dense "hot spot" in the immunoreactivity distribution
pattern in the area of the Golgi apparatus.
Figure 7. Immunofluorescence double-labelling of mast cells and nerve
fibers in human tissue pointing to possible interactions between the nervous
system and cutaneous peripheral cells. From H. Jacobi et al., in preparation.
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