Effects of Inflammatory Mediators on Gut Sensititvity
Over the past decade, attention has been paid to the role of visceral sensitivity in the pathophysiology of functional bowel disorders, especially irritable bowel syndrome, and visceral hypersensitivity is the most widely accepted mechanism responsible for both motor alterations and abdominal pain....
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| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
1999-01-01
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| Series: | Canadian Journal of Gastroenterology |
| Online Access: | http://dx.doi.org/10.1155/1999/846809 |
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| Summary: | Over the past decade, attention has been paid to the role of
visceral sensitivity in the pathophysiology of functional bowel disorders,
especially irritable bowel syndrome, and visceral hypersensitivity
is the most widely accepted mechanism responsible for
both motor alterations and abdominal pain. Inflammatory mediators
sensitize primary afferents, especially C-fibre polymodal nociceptors,
favouring the recruitment of silent nociceptors that give
rise to secondary spinal sensitization. After local tissue injury, the
release of chemical mediators such as potassium ions, ATP,
bradykinin and prostaglandin E2 directly activate nerve endings
and indirectly trigger the release of algesic mediators such as histamine,
5-hydroxytryptamine and nerve growth factor from other
cells, which, in turn, stimulate proximal afferent nerve endings
and silent nociceptors. Among the intermediary structures activated
by inflammatory mediators and susceptible to the release of
proalgesic substances, mast cells and platelets play a crucial role;
however, immunocytes such as macrophages and neutrophils or
sympathetic nerve terminals are also candidates. Moreover,
events likely to activate synthesis of mediators by mast cells, such
as stress and septic shock, also trigger colonic hypersensitivity.
Prolonged visceral hyperalgesia may also depend on spinal sensitization.
Anumber of substances are candidates to play a role at the
spinal cord level in mediating painful and nonpainful sensations.
Among them, substance P, dynorphins and glutamate play a pivotal
role in postsynaptic sensitization, particularly during and after
gut inflammation. Finally, despite the complexity of the relationship
between inflammatory mediators and gut hypersensitivity,
numerous results strongly suggest that alteration neuroimmune
communications at the gut level may trigger a series of events that
give rise to chronic changes in visceral sensitivity. |
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| ISSN: | 0835-7900 |