Premium
Experimental endotoxemia as a model to study neuroimmune mechanisms in human visceral pain
Author(s) -
Benson Sven,
Engler Harald,
Schedlowski Manfred,
Elsenbruch Sigrid
Publication year - 2012
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2012.06622.x
Subject(s) - visceral pain , context (archaeology) , neuroscience , medicine , immune system , pathophysiology , hyperalgesia , lipopolysaccharide , irritable bowel syndrome , chronic pain , inflammation , neuroimmunology , mechanism (biology) , sickness behavior , nociception , immunology , psychology , biology , receptor , philosophy , epistemology , paleontology
The administration of bacterial endotoxin (i.e., lipopolysaccharide, LPS) constitutes a well‐established experimental approach to study the effects of an acute and transient immune activation on physiological, behavioral, and emotional aspects of sickness behavior in animals and healthy humans. However, little is known about possible effects of experimental endotoxemia on pain in humans. This knowledge gap is particularly striking in the context of visceral pain in functional as well as chronic‐inflammatory gastrointestinal disorders. Although inflammatory processes have been implicated in the pathophysiology of visceral pain, it remains incompletely understood how inflammatory mediators interact with bottom–up (i.e., increased afferent input) and top–down (i.e., altered central pain processing) mechanisms of visceral hyperalgesia. Considering the recent findings of visceral hyperalgesia after LPS application in humans, in this review, we propose that experimental endotoxemia with its complex peripheral and central effects constitutes an experimental model to study neuroimmune communication in human pain research. We summarize and attempt to integrate relevant animal and human studies concerning neuroimmune communication in visceral and somatic pain, discuss putative mechanisms, and conclude with future research directions.