Persistent intestinal neuromuscular dysfunction after acute nematode infection in mice

Barbara, Giovanni; Collins, S. M.

doi:10.1053/gast.1997.v113.pm9322517

Cited by 186 publications

(135 citation statements)

References 3 publications

Supporting

Mentioning

124

Contrasting

Unclassified

Order By: Relevance

“…It has been reported that a greater number of EC cells is associated with visceral hypersensitivity in patients with IBS [40]. Experimental studies in animals support the findings that PI-IBS shows colonic hypercontractility during noxious stimulation of the gut [12,27], and our study confirms this in human IBS patients. Further prospective observations of the relationships between such a physiological exacerbation and changes in mucosal immunocyte infiltration [13,14], epithelial permeability [15] and composition of gut microbiome [41,42] are needed to confirm the hypothesis that the exaggerated motility responses to distention are mediated by persisting immune activation.…”

Section: Study Limitationssupporting

confidence: 89%

“…Animal studies have demonstrated that inflammation-induced intestinal muscle hypercontractility persists even after resolution of the inflammation [12,27] and that increases in muscle contractility are associated with increases in intestinal 5-HT and infiltration of immunocytes [28]. Several reports on histologic and immunohistochemical analyses in the intestinal mucosa [7,14,29] suggest that subtle morphologic changes involving lymphocytes, mast cells, enterochromaffin (EC) cells which contain serotonin, and enteric nerves may be associated with IBS symptoms.…”

Section: Colonic Motility Responses In Pi-ibsmentioning

confidence: 99%

“…Third, a mild transient gut inflammation led to long-term change of visceral hypersensitivity in an animal model of PI-IBS [11]. In another animal study, persistent intestinal smooth muscle hypercontractility was present after resolution of chemically induced inflammation [12]. It has been reported that colonic transit is accelerated in patients with PI-IBS compared to controls [13], but differences in phasic colon motility and smooth muscle tone have not been studied in humans with PI-IBS.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

670 Motility Response to Colonic Distention is Increased in Post-Infectious Irritable Bowel Syndrome (PI-IBS)

Kanazawa¹,

Palsson²,

Tilburg³

et al. 2010

Gastroenterology

View full text Add to dashboard Cite

Background-Acute intestinal infection leads to persistent intestinal smooth muscle hypercontractility and pain hypersensitivity after resolution of the infection in animal models. We investigated whether post-infectious irritable bowel syndrome (PI-IBS) is associated with abnormalities in phasic contractions of the colon, smooth muscle tone and pain sensitivity compared to non-PI-IBS (NI-IBS) or healthy controls (HC).

show abstract

Section: Study Limitationssupporting

confidence: 89%

Section: Colonic Motility Responses In Pi-ibsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

670 Motility Response to Colonic Distention is Increased in Post-Infectious Irritable Bowel Syndrome (PI-IBS)

Kanazawa¹,

Palsson²,

Tilburg³

et al. 2010

Gastroenterology

View full text Add to dashboard Cite

show abstract

“…Therefore, based on the previous and the present study it is possible that down-regulation of VIP in the jejunum is a long term effect and results from of processes other than nematode-evoked inflammation. It is likely that the observed VIP plasticity may be correlated with altered smooth muscle contractility which is observed in T. spiralis-infected mice even 42 days PI (Barbara et al, 1997). Since no signs of inflammation are seen 28 days PI, a hypothesis that transient T. spiralis infection leads to persistent gut dysfunction has been advanced (Bercik et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Expression of vasoactive intestinal polypeptide, substance P and neuropeptide Y in jejunal enteric nerves is altered in rabbits suffering from long term Trichinella spiralis infection: an immunohistochemical study

Arciszewski¹,

Nowakowski²,

Wąsowicz³

et al. 2009

Vet. Med. - Czech

View full text Add to dashboard Cite

ABSTRACT:In the early intestinal stage of infection with the nematode Trichinella spiralis alterations in gut motility and chemical code of enteric neurons are observed. The present study was designed to characterize the changes in expression pattern of vasoactive intestinal polypeptide (VIP), substance P (SP) and neuropeptide Y (NPY) in enteric nerves of the rabbit jejunum occurring during long-lasting trichinellosis (35 and 42 days). Sections of the jejunum from healthy and T. spiralis-infected rabbits were processed for double immunocytochemistry in which antibodies against protein gene product 9.5 were used as a pan-neuronal marker and mixed with antisera raised against VIP, SP or NPY. At 35 and 42 days post infection a marked decrease of VIP-, SP-and NPY-immunoreactive (IR) jejunal myenteric neurons was found, whereas the expression of these neuropeptides in submucous neurons was unchanged. In the myenteric plexus and the jejunal circular muscle of T. spiralis-infected rabbits a significant reduction of VIP-IR (but not SP-IR) nerve fibres was noted. In the longitudinal muscle of the jejunum from animals with long-lasting trichinellosis the density of SP-IR nerve terminals was decreased, whereas the number of VIP-containing nerve fibres was unchanged. Long-lasting trichinellosis had no influence on NPY-IR nerve fibres in both circular and longitudinal smooth muscles. The number of NPY-positive (but not VIP-and SP-IR) nerve fibres supplying mucosa and blood vessels was decreased in T. spiralis-infected animals. These data indicate that during long-lasting trichinellosis expression of neuropeptides in jejunal enteric neurons is changed. A possible involvement of VIP and SP in persistent intestinal dysmotility and NPY in altered fluid secretion is discussed.

show abstract

“…This evidence, based on extensive study of the Trichinella-infected jejunum of small experimental animals (Collins 1996;Barbara et al 1997) is supported by several studies in IBS that demonstrate increased numbers of intra-mucosal inflammatory cells including __________________________________________________________________________________ 21 mast cells (Barbara et al 2004;Wang et al 2004) and T lymphocytes (Spiller et al 2000;Chadwick et al 2002), as well as increased levels of pro-inflammatory mediators (Gonsalkorale et al 2003;O'Mahony et al 2005). Inflammatory cells have also been…”

Section: The Gi Tract As a Target For Autoimmunitymentioning

confidence: 72%

The role of humoral autoimmunity in gastrointestinal neuromuscular diseases

Hubball

Martin

Lang

et al. 2009

Progress in Neurobiology

View full text Add to dashboard Cite

Dysfunction of the gastrointestinal neuromuscular apparatus (including interstitial cells ofCajal) is presumed to underlie a heterogeneous group of disorders collectively termed gastrointestinal neuromuscular diseases (GINMDs). Humoral (antibody)-mediated autoimmunity directed against ligand-or voltage-gated ion channels or associated proteins involved in neuromuscular transmission is associated with several acquired neuromuscular diseases of the periphery and is now implicated in an increasing number of less well-characterised diseases. Anti-channel antibodies have been reported in small numbers of patients with GINMD, particularly in those with GI dysfunction secondary to an underlying disease such as neoplasia or infection. However, little is known of humoral autoimmunity in primary GINMDs.This thesis investigated the association between anti-channel antibodies and GINMD, and the human GI tract as a potential target of anti-channel antibodies. The presence of antivoltage-and ligand-gated antibodies was investigated in the serum of patients with primary achalasia, enteric dysmotility and intestinal pseudo-obstruction, and in those with GINMD secondary to Chagas' disease. The functional effect of sera from some of these patients on colonic smooth muscle contractility was also characterised. Finally, the distribution of six voltage-gated potassium channels (VGKCs), which serve essential roles in the peripheral and central nervous systems and are known targets of pathological autoantibodies, were investigated in all layers of the human GI tract.Our findings suggest that currently recognised anti-channel antibodies are not a common pathogenic factor in primary GINMDs. Anti-channel antibodies, in particular anti-VGKC antibodies, were however found in a significant number of individuals with Chagas' disease. Furthermore, circulating factors in patients with chagasic GI disease altered GI smooth muscle contractility in vitro which may have pathological relevance to GI

show abstract

Persistent intestinal neuromuscular dysfunction after acute nematode infection in mice

Cited by 186 publications

References 3 publications

670 Motility Response to Colonic Distention is Increased in Post-Infectious Irritable Bowel Syndrome (PI-IBS)

670 Motility Response to Colonic Distention is Increased in Post-Infectious Irritable Bowel Syndrome (PI-IBS)

Expression of vasoactive intestinal polypeptide, substance P and neuropeptide Y in jejunal enteric nerves is altered in rabbits suffering from long term Trichinella spiralis infection: an immunohistochemical study

The role of humoral autoimmunity in gastrointestinal neuromuscular diseases

Contact Info

Product

Resources

About