Systematic review of animal models of post-infectious/post-inflammatory irritable bowel syndrome

Qin, Hongjiu; Wu, Justin Che Yuen; Tong, Xu; Sung, Joseph J.Y.; Hong, Xu; Bian, Zhaoxiang

doi:10.1007/s00535-010-0321-6

Cited by 91 publications

(75 citation statements)

References 105 publications

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“…This colitis is transient, peaking several days after administration and then spontaneously healing such that by 28 days following administration the histology of the colon and myeloperoxidase levels do not differ from untreated animals (Hughes et al, 2009a;Hughes et al, 2009b;Krauter et al, 2007;Qin et al, 2011). However, colonic afferent nerves remain sensitized to distension long after the mucosa heals, which models aspects of the chronic visceral hypersensitivity (CVH) experienced by IBS patients (Gschossmann et al, 2004;Hughes et al, 2009a;Hughes et al, 2009b).…”

Section: Introductionmentioning

confidence: 99%

Immune derived opioidergic inhibition of viscerosensory afferents is decreased in Irritable Bowel Syndrome patients

Hughes

Moretta

Lim

et al. 2014

Brain, Behavior, and Immunity

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Immune derived opioidergic inhibition of viscerosensory afferents is decreased in Irritable Bowel Syndrome patients, Brain, Behavior, and Immunity (2014), doi: http://dx.doi.org/10. 1016/j.bbi.2014.07.001 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. supernatants from HS and IBS patients were applied to colo-rectal sensory afferent endings in mice with post-inflammatory chronic visceral hypersensitivity (CVH). β-endorphin was identified predominantly in monocyte / macrophages relative to T or B cells in human PBMC and colonic lamina propria. Monocyte derived β-endorphin levels and colonic macrophage numbers were lower in IBS patients than healthy subjects. PBMC supernatants from healthy subjects had greater inhibitory effects on colo-rectal afferent mechanosensitivity than those from IBS patients. The inhibitory effects of PBMC supernatants were more prominent in CVH mice compared to healthy mice due to an increase in µ-opioid receptor expression in dorsal root ganglia neurons in CVH mice. Monocyte / macrophages are the predominant immune cell type responsible for β-endorphin secretion in humans. IBS patients have lower monocyte derived β-endorphin levels than healthy subjects, causing less inhibition of colonic afferent endings. Consequently, altered immune function contributes toward visceral hypersensitivity in IBS.

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Section: Introductionmentioning

confidence: 99%

Immune derived opioidergic inhibition of viscerosensory afferents is decreased in Irritable Bowel Syndrome patients

Hughes

Moretta

Lim

et al. 2014

Brain, Behavior, and Immunity

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“…Delivered at different phases of the life cycle, such stressors may trigger risk factors for visceral hypersensitivity. Accumulating evidence suggests that the internal and external validity of such models is adequate particularly with regard to species, specific gender, age and strain (Larauche et al, 2011;Qin et al, 2011). In contrast to human studies, in which self-reported responses to gut distension can be measured, pseudoaffective markers of the nociception in animal studies are needed.…”

Section: Irritable Bowel Syndromementioning

confidence: 99%

Assessment and manifestation of central sensitisation across different chronic pain conditions

Arendt-Nielsen

Morlion

Perrot

et al. 2017

European Journal of Pain

483

494

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Different neuroplastic processes can occur along the nociceptive pathways and may be important in the transition from acute to chronic pain and for diagnosis and development of optimal management strategies. The neuroplastic processes may result in gain (sensitisation) or loss (desensitisation) of function in relation to the incoming nociceptive signals. Such processes play important roles in chronic pain, and although the clinical manifestations differ across condition processes, they share some common mechanistic features. The fundamental understanding and quantitative assessment of particularly some of the central sensitisation mechanisms can be translated from preclinical studies into the clinic. The clinical perspectives are implementation of such novel information into diagnostics, mechanistic phenotyping, prevention, personalised treatment, and drug development. The aims of this paper are to introduce and discuss (1) some common fundamental central pain mechanisms, (2) how they may translate into the clinical signs and symptoms across different chronic pain conditions, (3) how to evaluate gain and loss of function using quantitative pain assessment tools, and (4) the implications for optimising prevention and management of pain. The chronic pain conditions selected for the paper are neuropathic pain in general, musculoskeletal pain (chronic low back pain and osteoarthritic pain in particular), and visceral pain (irritable bowel syndrome in particular). The translational mechanisms addressed are local and widespread sensitisation, central summation, and descending pain modulation. Significance Central sensitisation is an important manifestation involved in many different chronic pain conditions. Central sensitisation can be different to assess and evaluate as the manifestations vary from pain condition to pain condition. Understanding central sensitisation may promote better profiling and diagnosis of pain patients and development of new regimes for mechanism based therapy. Some of the mechanisms underlying central sensitisation can be translated from animals to humans providing new options in development of therapies and profiling drugs under development.

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“…Intracolonic 2,4,6-trinitrobenzene sulfonic acid (TNBS) in rodents has been widely used as a model of colitis (23), and recently TNBS has been advanced as a model of postinflammatory colorectal hypersensitivity and thus a model of PI-IBS (20). Hughes et al (14) reported, for example, an inflammation-associated increase in colorectal afferent sensitization and a long-lasting sensitization of serosal and mesenteric class afferents after resolution of TNBS-induced colorectal inflammation.…”

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confidence: 99%

Altered colorectal afferent function associated with TNBS-induced visceral hypersensitivity in mice

Feng

Tanaka

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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Feng B, La JH, Tanaka T, Schwartz ES, McMurray TP, Gebhart GF. Altered colorectal afferent function associated with TNBS-induced visceral hypersensitivity in mice. Am J Physiol Gastrointest Liver Physiol 303: G817-G824, 2012. First published August 1, 2012; doi:10.1152/ajpgi.00257.2012.-Inflammation of the distal bowel is often associated with abdominal pain and hypersensitivity, but whether and which colorectal afferents contribute to the hypersensitivity is unknown. Using a mouse model of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis, we investigated colorectal hypersensitivity following intracolonic TNBS and associated changes in colorectum and afferent functions. C57BL/6 mice were treated intracolonically with TNBS or saline. Visceromotor responses to colorectal distension (15-60 mmHg) were recorded over 8 wk in TNBS-and saline-treated (control) mice. In other mice treated with TNBS or saline, colorectal inflammation was assessed by myeloperoxidase assay and immunohistological staining. In vitro single-fiber recordings were conducted on both TNBS and saline-treated mice to assess colorectal afferent function. Mice exhibited significant colorectal hypersensitivity through day 14 after TNBS treatment that resolved by day 28 with no resensitization through day 56. TNBS induced a neutrophil-and macrophage-based colorectal inflammation as well as loss of nerve fibers, all of which resolved by days 14 -28. Single-fiber recordings revealed a net increase in afferent drive from stretch-sensitive colorectal afferents at day 14 post-TNBS and reduced proportions of mechanically insensitive afferents (MIAs) at days 14 -28. Intracolonic TNBS-induced colorectal inflammation was associated with the development and recovery of hypersensitivity in mice, which correlated with a transient increase and recovery of sensitization of stretch-sensitive colorectal afferents and MIAs. These results indicate that the development and maintenance of colorectal hypersensitivity following inflammation are mediated by peripheral drive from stretch-sensitive colorectal afferents and a potential contribution from MIAs. electrophysiology; IBS; PI-IBS; single-fiber; visceral pain IRRITABLE BOWEL SYNDROME (IBS) is a functional gastrointestinal disorder characterized by persistent pain and organ hypersensitivity in the absence of demonstrable gross structural or biochemical abnormalities. Although the cause(s) of IBS is unclear, postinfectious IBS (PI-IBS) seems to have a defined etiology because in those patients, an infectious gastroenteritis precedes the development of IBS symptoms (22).Intracolonic 2,4,6-trinitrobenzene sulfonic acid (TNBS) in rodents has been widely used as a model of colitis (23), and recently TNBS has been advanced as a model of postinflammatory colorectal hypersensitivity and thus a model of . Hughes et al. (14) reported, for example, an inflammation-associated increase in colorectal afferent sensitization and a long-lasting sensitization of serosal and mesenteric class afferents after resolution of TNBS-in...

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Systematic review of animal models of post-infectious/post-inflammatory irritable bowel syndrome

Cited by 91 publications

References 105 publications

Immune derived opioidergic inhibition of viscerosensory afferents is decreased in Irritable Bowel Syndrome patients

Immune derived opioidergic inhibition of viscerosensory afferents is decreased in Irritable Bowel Syndrome patients

Assessment and manifestation of central sensitisation across different chronic pain conditions

Altered colorectal afferent function associated with TNBS-induced visceral hypersensitivity in mice

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