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cords transected proximally have exaggerated inflammatory responses
[23]
. Further-
more, there is convincing evidence that stress can activate mast cells to degranulate
and support neurogenic inflammation. Upon emotional excitement, autonomic nerves
convey these stimuli to primary afferent sensory nerves that transmit the impulses
antidromically, resulting in the release of various neuropeptides from sensory nerve
endings and degranulation of mast cells
[24]
. This is the presumed basis of psy-
chogenic urticaria. That the brain can cause mast-cell degranulation is also evident
from experimental studies which demonstrated that acute psychological stress in
rats (induced by immobilization) leads to mast-cell degranulation in the dura, blad-
der, and intestine
[7]
. Furthermore, isolation stress has been shown to cause mast-
cell degranulation in the skin. This was mediated by the inflammatory neuropeptides
SP, corticotrophin releasing factor (CRF), and neurotensin—mediators that are
known to induce neurogenic inflammation
[25]
.
Moreover, many skin disorders, such as atopic dermatitis and psoriasis, worsen
during stress and are associated with increased numbers and activation of mast
cells, which release vasoactive, nociceptive, and pro-inflammatory mediators
[26]
.
Furthermore, migraine headache is often precipitated by stress. Kandere-Grzybowska
et al. demonstrated, in various experimental studies with knockout mice, that acute
restraint stress resulted in increased dura mast-cell activation through the activation
of NK-1 receptors by neuropeptides. The fact that SP -/- mice had intact vascular
permeability response to stress indicates that some other NK-1 receptor agonist may
substitute for SP
[27]
.
The number of activated mast cells is also increased in the adventitia of coronary
segments with plaque rupture and in spastic atherosclerotic coronary segments. Laine
et al. identified and quantified contacts between mast cells and nerves in the adven-
titia of normal and atherosclerotic coronary segments. The authors concluded that
neurogenic stimulation of mast cells in the adventitia of coronary arteries may induce
the release of vasoactive compounds, such as histamine and leukotrienes, which can
contribute to the complex neurohormonal response that leads to abnormal coronary
vasoconstriction
[28]
.
In summary, there is cumulative evidence that mast cells, which connect neuro-
genic and immunological inflammation, can be activated by psychological stress. In
this context, stress can influence a variety of inflammatory diseases in the skin and
the joints, as well as in the cardiopulmonary, urinary, and nervous systems. Hence,
we know that psychological factors can precipitate or increase the morbidity of dis-
eases mediated by neurogenic inflammation
[25]
.
8.2 The “Inflammatory Reflex”: A Mechanism to
Counter-Regulate Immunological Inflammation
In the scenario of immunological inflammation, microbial signals, as well as host
cell products that are altered (e.g., fragmented matrix proteins or oxidized lipopro-
teins), abnormally released (e.g., heat shock proteins), or released in abnormally
