Extrinsic and intrinsic neurons of the gut contain multiple neuropepti
des, which through complex interactions modulate mucosal defense, infl
ammation, and repair in response to injury. Initial changes of the neu
rovascular peptidergic system may represent normal protective mechanis
ms against tissue injury, whereas subsequent alterations of neurovascu
lar regulation may contribute to the pathogenesis and maintenance of t
he inflammatory state. Multiple interactions between sensory neurons,
the immune system and growth factors appear to exist, and then is also
a marked plasticity of the neurovascular peptidergic system with chan
ges in the synthesis, release, binding, and degradation of peptides du
ring inflammatory processes. A delicate and closely regulated balance
between proinflammatory (e.g., SP, VIP, NPY) and antiinflammatory neur
opeptides (e.g., CGRP, somatostatin, bombesin) seems to exist in the g
astrointestinal tract. Disturbances of this balance might contribute t
o the pathophysiology of inflammatory bowel disease. In our overview,
we will describe the results of studies in animal models of experiment
al inflammation and focus on the potential insight they provide in und
erstanding the pathophysiology of inflammatory conditions of the bowel
such as IBD. Knowledge with respect to these regulatory systems might
provide novel insights into the inflammatory process and potentially
expand the available therapeutic approaches in the management of IBD.