2007
DOI: 10.1007/s10620-007-9881-6
|View full text |Cite
|
Sign up to set email alerts
|

Visceral and Somatic Hypersensitivity in TNBS-Induced Colitis in Rats

Abstract: Inflammation of visceral structures in rats has been shown to produce visceral/somatic hyperalgesia. Our objectives were to determine if trinitrobenzene sulfonic acid (TNBS) induced colitis in rats leads to visceral/somatic hypersensitivity. Male Sprague-Dawley rats (200g-250g) were treated with 20 mg of TNBS in 50% ethanol (n=40) or an equivalent volume of ethanol (n=40) or saline (n=25) via the colon. Colonic distension, Von-Frey, Hargreaves, and tail reflex test were used to evaluate for visceral, mechanica… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

2
38
0
1

Year Published

2010
2010
2023
2023

Publication Types

Select...
4
2
1

Relationship

0
7

Authors

Journals

citations
Cited by 50 publications
(41 citation statements)
references
References 50 publications
2
38
0
1
Order By: Relevance
“…The results suggest that immune activation, the main pathogenesis of IBD, may also contribute to symptom generation in IBS patients. Furthermore, animal studies have shown that the animals' intestinal sensory-motor system was altered after the induction of experimental colitis, and that the changes persisted even after inflammation resolution [16,62,79,90]; this suggests that the occurrence of IBD may be linked with the development of IBS. These findings support the hypothesis that chemical agent-induced inflammation and recovery can, to some extent, mimic the development of IBS in patients recovering from acute gastroenteritis or IBD [106].…”
Section: Discussionmentioning
confidence: 99%
See 2 more Smart Citations
“…The results suggest that immune activation, the main pathogenesis of IBD, may also contribute to symptom generation in IBS patients. Furthermore, animal studies have shown that the animals' intestinal sensory-motor system was altered after the induction of experimental colitis, and that the changes persisted even after inflammation resolution [16,62,79,90]; this suggests that the occurrence of IBD may be linked with the development of IBS. These findings support the hypothesis that chemical agent-induced inflammation and recovery can, to some extent, mimic the development of IBS in patients recovering from acute gastroenteritis or IBD [106].…”
Section: Discussionmentioning
confidence: 99%
“…The TNBS-induced PI-IBS model has been well studied, and the features of IBS, such as visceral hypersensitivity [16,[18][19][20][21][22][23][24][25][26][27][28][29]36], motility dysfunction [30], alteration in histopathology [33][34][35], and changes in permeability and secretion [31,32], have also been identified in the experimental animals after recovery from the initial inflammation. Moreover, studies have indicated that TNBS-induced visceral hypersensitivity is long-lasting (about 17 weeks after TNBS administration), and that the effects of TNBS are dose dependent [18,19].…”
Section: Trinitrobenzene Sulfonic Acidmentioning
confidence: 99%
See 1 more Smart Citation
“…In this respect the most important cytokine is tumor necrosis factor-alpha (TNF-α), which participates in a complex network of interactions in both acute and chronic inflammation (Gross et al 1991;Niederau et al 1997). TNF-α, produced from different types of leukocytes, is the proximal cytokine generated during an inflammatory response; it is capable of activating other cytokines and hence, remaining at the focus of the inflammation, inducing the development of a microcirculatory disturbance and excessive, systemic inflammation (Zhou et al 2006;Zhou et al 2008). …”
Section: Characteristics Of Inflammationmentioning
confidence: 99%
“…A single intracolonic enema of TNBS causes transmural colitis, which lasts longer than 8 weeks, and reproduces several symptoms of human IBD (Morris 1989). This model is characterized by a weight loss (Morris 1989) with visceral hyperalgesia (Zhou 2008), significant elevations of the proinflammatory cytokines, including TNF-α (Neurath 1997) and interleukin-6 (IL-6) (Hove 2001), extensive ulcerations, morphological changes (Tatsumi 1996) and tissue leukocyte accumulation (Kiss 1997).…”
Section: Experimental Models Of Human Ibdmentioning
confidence: 99%