Biology Reference
In-Depth Information
deposited at the site of injury, platelets aggregate and become activated, and the red cells
stack together to help stop bleeding. The dead and dying cells contribute to pus formation.
3.
Termination
of inflammatory response by specific inhibitors. Over the next days, resolution
may occur, meaning that the inflammation will stop because of a counter-regulatory anti-
inflammatory response leading to release of the powerful anti-inflammatory cytokine IL-10
and transforming growth factor (TGF)-. Furthermore, repair processes start and various
growth factors are produced. If it is not possible to return the tissue to its original form,
scarring
is generated by fibroblasts, collagen, and new endothelial cells.
However, when the ability to remove foreign materials is impaired, or regulation
is altered, inflammation may become harmful to the host. In this situation the innate
immune response may cause cell and tissue damage and hence multiple organ fail-
ure, which is known as
sepsis
. Inflammation may be excessive and totally inappropri-
ate (e.g., in allergy, autoimmune diseases, sepsis), and sometimes the inflammatory
response cannot terminate and becomes chronic
[1-3]
.
A number of inflammatory stimuli (toxins, antigens, bacterial and chemical mate-
rial, etc.) have been identified. These stimuli can interact with cell receptors cre-
ated after a sensitizing exposure to trigger an inflammatory cascade that induces
host defense. In this scenario,
neurogenic inflammation
occurs: this is defined as a
process by which inflammation is triggered by the nervous system. This means that
nerve cells recognize a stimulus and initiate the inflammatory response independent
from the immune system. This is called the
inflammatory spinal reflex
[4-6]
(
Figure
8.1
). Further progress of the response depends on the type of the inflammatory stimulus.
For example, chemical toxins may induce inflammation only by neuronal effects.
However, bacterial materials may in parallel initiate an
immunological inflammation.
Alternatively, neurogenic inflammation may evolve into immunological inflamma-
tion. Thus, a close relationship exists between somatic and autonomic nerves and
inflammatory cells, especially mast cells, during the course of inflammation
[7]
.
Most of the evidence for neurogenic inflammation has been derived from stud-
ies of fine unmyelinated (C-) or myelinated (A-) fibers, which derive from the
dorsal root ganglia and can be activated by various chemical or biochemical toxins.
Stimulation of these fibers leads to the release of various neuropeptides from periph-
eral nerve terminals.
Neuropeptides
are a group of small peptides with 4 to more than 40 amino acids.
More than 20 neuropeptides have been identified. However, regarding the function
of a neuropeptide, organ- and species-specific effects must be considered. The most
recognized neuropeptides are substance P (SP), neurokinin (NK)- A, neurotensin, cal-
citonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP), pituitary ade-
nylate cyclase-activating polypeptide (PACAP), neuropeptide Y, somatostatin (SOM),
-endorphin, enkephalin, galanin, dynorphin, atrial natriuretic peptide, melanocyte-
stimulating hormone (MSH), parathyroid hormone-related protein, corticotropin-releasing
hormone (CRH), and urocortin
[7]
. Under physiologic conditions, immune, tissue, and
neural cells are all capable of producing and releasing neuropeptides.
In neurogenic inflammation, the release of SP, CGRP, NK-A, NK-B, and soma-
tostatin from nerve endings leads to extravasation from postcapillary venules and
