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Moreover, vagus nerves supply most of the sensory fibers to different organs, for
example the airways. Inappropriate activation of these nerves can lead to many of
the symptoms of allergic and chronic obstructive pulmonary disease, such as cough-
ing, mucus hypersecretion, and bronchoconstriction
[17]
. The afferent sensory fibers,
which contain neuropeptides—in particular CGRP, SP, and NK-A—have receptors
sensitive to bradykinin, hypertonic saline, low chloride, cigarette smoke, and ozone.
The sensory nerve activity may be enhanced during airway inflammation (e.g.,
bronchitis) so that protective central and local reflexes become exacerbated and del-
eterious, and may contribute to the pathophysiology and symptomatology of airway
inflammatory diseases, such as asthma and chronic obstructive pulmonary disease
(COPD)
[17,19]
. Similarly, inappropriate activation of trigeminal afferent nerves,
comparable to the vagal afferent nerves innervating the lower airways, leads to many
of the symptoms associated with allergic rhinitis (including sneezing, mucus secre-
tion, vascular engorgement, and plasma exudation). The mechanisms involved in
the increased responsiveness of sensory nerves under inflammatory conditions are
not completely known. However, there is evidence that interactions of inflamma-
tory mediators (e.g., PG, bradykinin) with sensory and autonomic nerves lead to an
increase in neurotransmitter release
[19]
.
Neurogenic inflammation and its interference with immunological inflammation,
as well as the impairment of control mechanisms due to psychological stress, are
co-factors in the development of chronic inflammatory diseases such as asthma, rhinitis,
rheumatoid arthritis, and migraine headache. It is interesting that organs with a high
density of neuropeptide receptors, such as the intestines and the lungs, have been pro-
posed to be more susceptible to perturbations from inflammation
[20]
. Indeed, ner-
vous innervation of an organ is a requirement for establishing certain inflammatory
reactions experimentally
[21]
. For example, Levine et al. found, in a rat model, that
joints developed more severe arthritis following injection of Freund's adjuvant into
the footpad when they were more densely innervated by SP-containing primary affer-
ent neurons. Infusion of SP into the knee increased the severity of arthritis, whereas
the injection of SP receptor antagonist did not. These results suggest a significant
physiological difference between joints that develop mild and severe arthritis, and
indicate that the release of intraneuronal SP contributes to the severity of arthritis.
Moreover, if the nerve innervating a joint was cut, arthritis could not be induced in the
denervated joint
[22]
. This is reminiscent of clinical cases in which rheumatoid arthri-
tis resolves on the side affected by a cerebral ischemia and following hemiplegia
[22]
.
Another disorder that increases significantly over time is migraine headaches. On
the basis of pharmaceutical responses of migraine and animal experiments, it is sup-
posed that neurogenic inflammation plays a role in the pathophysiology of migraine
headaches. It was demonstrated in a rat model that stimulation of trigeminal sensory
fibers leads to changes consistent with those of migraine, and that these changes
could be blocked by the serotonin antagonists; these results suggest that neurogenic
inflammation mediates migraine
[5]
.
The activation of sensory neurons as a key mechanism of neurogenic inflamma-
tion is also under the control of supraspinal neurons and descending spinal tracts,
which may down-regulate the reaction. This is why “spinal” animals with spinal
