scholarly journals Brain-Gut Interactions in Inflammatory Bowel Disease: Mechanisms of Anorexia in Animal Models of Experimental Colitis

1996 ◽  
Vol 10 (5) ◽  
pp. 329-334
Author(s):  
Harvey P Weingarten
Keyword(s):  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Bowel Disease ◽  
Cytokine Production ◽  
Experimental Colitis ◽  
Physiological Processes ◽  
Disease Mechanisms ◽  
The Central Nervous System ◽  
Inflammatory Bowel ◽  
The Brain

Physiological processes within the bowel are influenced constantly by signals from other organs, primarily the brain. The mechanisms by which inflammation of the gastrointestinal tract results in anorexia are unknown. Understanding how the inflammation-related signals in the periphery are communicated to the central nervous system and activate cytokine production in the brain remains an enormous challenge. Elucidation of these gut-brain communication mechanisms is essential to the development of appropriate and efficacious treatments for the eating and weight disturbances associated with inflammatory bowel disease.

scholarly journals Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease

2022 ◽  
Vol 19 (1) ◽  
Author(s):  
Colin F. Craig ◽  
Rhiannon T. Filippone ◽  
Rhian Stavely ◽  
Joel C. Bornstein ◽  
Vasso Apostolopoulos ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Bowel Disease ◽  
Structural Changes ◽  
Intestinal Inflammation ◽  
In Vivo Models ◽  
The Central Nervous System ◽  
Inflammatory Bowel

AbstractPatients with inflammatory bowel disease (IBD) suffer from depression at higher rates than the general population. An etiological trigger of depressive symptoms is theorised to be inflammation within the central nervous system. It is believed that heightened intestinal inflammation and dysfunction of the enteric nervous system (ENS) contribute to impaired intestinal permeability, which facilitates the translocation of intestinal enterotoxins into the blood circulation. Consequently, these may compromise the immunological and physiological functioning of distant non-intestinal tissues such as the brain. In vivo models of colitis provide evidence of increased blood–brain barrier permeability and enhanced central nervous system (CNS) immune activity triggered by intestinal enterotoxins and blood-borne inflammatory mediators. Understanding the immunological, physiological, and structural changes associated with IBD and neuroinflammation may aid in the development of more tailored and suitable pharmaceutical treatment for IBD-associated depression.

scholarly journals Putative Metronidazole Neurotoxicosis in a Cat

2005 ◽  
Vol 42 (5) ◽  
pp. 665-669 ◽  
Author(s):  
E. J. Olson ◽  
S. C. Morales ◽  
A. S. McVey ◽  
D. W. Hayden
Keyword(s):  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Supportive Care ◽  
Bowel Disease ◽  
Clinical Signs ◽  
Histologic Evaluation ◽  
The Central Nervous System ◽  
Inflammatory Bowel ◽  
Adult Cat

A presumptive case of metronidazole toxicity in a 3.4-kg adult cat is described. The cat had been treated for suspected inflammatory bowel disease with an anti-inflammatory dose of prednisone and metronidazole (73.5-147 mg/kg PO q24h) for approximately 40 days prior to presentation. Clinical signs were primarily related to the central nervous system, including acute tetraparesis, unresponsiveness, tremors, and vocalization. The patient was euthanatized after 12 days of supportive care. Necropsy revealed no significant macroscopic lesions. Histologic evaluation revealed multifocal, fairly well-demarcated foci of necrosis in the brainstem, extending from the diencephalon to the medulla oblongata. To our knowledge, this is the first report to document histologic lesions associated with metronidazole administration in a cat.

scholarly journals Inflammatory Bowel Disease: Mechanisms, Redox Considerations, and Therapeutic Targets

2013 ◽  
Vol 19 (14) ◽  
pp. 1711-1747 ◽  
Author(s):  
Fiorella Biasi ◽  
Gabriella Leonarduzzi ◽  
Patricia I. Oteiza ◽  
Giuseppe Poli
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Therapeutic Targets ◽  
Disease Mechanisms ◽  
Inflammatory Bowel

Up-regulation of inducible co-stimulator (ICOS) expression and its regulation of cytokine production in inflammatory bowel disease

2000 ◽  
Vol 118 (4) ◽  
pp. A662
Author(s):  
Toshirou Sato ◽  
Manoru Watanabe ◽  
Takanori Kanai ◽  
Akira Okazawa ◽  
Hanae Takagi ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Cytokine Production ◽  
Inflammatory Bowel

Inflammatory Bowel Disease and Risk of Birth Defects in Offspring

2020 ◽  
Vol 14 (5) ◽  
pp. 588-594
Author(s):  
Nathalie Auger ◽  
Justin Côté-Daigneault ◽  
Marianne Bilodeau-Bertrand ◽  
Laura Arbour
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Birth Defects ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Central Nervous System Defects

Abstract Background and Aims The relationship between inflammatory bowel disease in pregnancy and birth defects is not understood. We evaluated whether Crohn’s disease and ulcerative colitis in pregnant women were associated with the risk of birth defects in the offspring. Methods We undertook a retrospective cohort study of 2 184 888 pregnancies in Quebec, Canada, between 1989 and 2016. We calculated risk ratios [RR] and 95% confidence intervals [CI] for the association between inflammatory bowel disease and the risk of birth defects, using generalised estimating equations adjusted for maternal characteristics. We assessed associations in the period before 2000, when immunosuppressive biologic therapy and folic acid food fortification were not yet available, compared with the period after 2000 when these interventions were more widespread. Results This study included 13 099 women with Crohn’s disease and 7798 with ulcerative colitis. Crohn’s disease was associated with 1.90 times [95% CI 1.10–3.28] the risk of abdominal wall defects [gastroschisis, omphalocoele, and diaphragmatic hernia] and ulcerative colitis was associated with 1.53 times [95% CI 1.02–2.30] the risk of central nervous system defects. The association of Crohn’s disease with abdominal wall defects was stronger before 2000 [RR 3.62, 95% CI 1.71–7.67] than after 2000 [RR 1.23, 95% CI 0.55–2.75]. Ulcerative colitis was associated with central nervous system defects regardless of time period. Conclusions These findings suggest that inflammatory bowel disease is associated with the risk of abdominal wall and central nervous system defects, and that introduction of immunobiologic medications is unlikely to be associated with added risk. Podcast This article has an associated podcast which can be accessed at https://academic.oup.com/ecco-jcc/pages/podcast

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