Ulcerative colitis

Farrell, Richard J.; Peppercorn, Mark A.

doi:10.1016/s0140-6736(02)07499-8

Cited by 257 publications

(215 citation statements)

References 137 publications

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“…Chronic inflammatory bowel disease (IBD) is a multifactorial disorder that is characterized by inflammation specific to the gastrointestinal tract, which results in intestinal malabsorption, immune defense abnormalities, and an exaggerated inflammatory response (1,2). Various immune and inflammatory cells, such as lymphocytes, macrophages, and dendritic cells, play important roles in the development and progression of IBD (3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, bacterial antigens have been implied in the pathological inflammation and may mediate both innate and adaptive responses underlying chronic inflammation (6)(7)(8). IBD consists of two main subtypes: ulcerative colitis (UC) and Crohn's disease (CD) (1,2). Although the precise etiology of IBD remains unknown, both several environmental factors, such as dietary components and microorganisms, and genetic factors may contribute to the occurrence of IBD (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

“…RA is involved in autoimmune diseases, of which pathoetiology is probably similar to UC in a number of respects with not only mechanisms of immune defense abnormalities, such as the elevated production of autoantibody (1,2), but also arthritic manifestations, e.g. ankylosing spondylitis and sacroiliitis (11).…”

Section: Introductionmentioning

confidence: 99%

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Haplotypes of PADI4 susceptible to rheumatoid arthritis are also associated with ulcerative colitis in the Japanese population

Chen

Isomoto

Narumi

et al. 2008

Clinical Immunology

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Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is a chronic inflammatory disorder characterized by intractable inflammation specific to the gastrointestinal tract. The precise etiology of IBD remains unknown. Recently, haplotypes of peptidylarginine deiminase type 4 (PADI4) have been identified as the rheumatoid arthritis (RA)-susceptible gene. PADI4 is located at 1p36, which is one of chromosomal loci susceptible for IBD. Then, we examined whether haplotypes and diplotypes of PADI4 are associated with IBD in the Japanese population. We studied haplotypes of PADI4 in 114 patients with UC, 83 patients with CD, and 200 gender-matched healthy controls by PCR-restriction fragment length polymorphism. Frequencies and distributions of haplotypes and diplotypes were compared statistically between patients and controls by logistic regression analysis. The frequency of haplotype 1 was significantly decreased in patients with UC, compared to that in controls (P = 0.037; odds ratio (OR) = 0.702). In contrast, the frequency of haplotype 2 in patients with UC was significantly higher than that in controls (P = 0.003; OR = 1.722). Moreover, of a total of 114 patients with UC, 15 (13.2%) had a diplotype homozygous for haplotype 2, the frequency being significantly higher than in controls (9/200, 4.5%; P = 0.008, OR = 3.215). Our results indicate that Czin 4 haplotype 1 of PADI4 is associated with non-susceptibility to UC, whereas haplotype 2 is susceptible to UC. Thus, it is likely that PADI4 is one of genetic determinants of UC in the Japanese population.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Haplotypes of PADI4 susceptible to rheumatoid arthritis are also associated with ulcerative colitis in the Japanese population

Chen

Isomoto

Narumi

et al. 2008

Clinical Immunology

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“…Vasopressin neurons in the PVN, particularly its parvocellular sub-nuclei, innervate the NTS. The fiber tracts descending from the PVN transport AVP to the NTS [15,16] . In situ hybridization studies and autoradiographic binding assays have demonstrated the presence of AVP V 1 -receptor mRNA and dense V 1 -receptors in the NTS [17] .…”

Section: Introductionmentioning

confidence: 99%

Glutamate microinjection into the hypothalamic paraventricular nucleus attenuates ulcerative colitis in rats

Zhang

Fei

et al. 2013

Acta Pharmacol Sin

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Aim: To investigate the effects of glutamate microinjection into hypothalamic paraventricular nucleus (PVN) on ulcerative colitis (UC) in rats and to explore the relevant mechanisms. Methods: 2,4,6-Trinitrobenzenesulfonic acid (100 mg/kg in 50% ethanol) was instilled into the colon of adult male SD rats to induce UC. A colonic damage score (CDS) was used to indicate the severity of the colonic mucosal damage. The pathological changes in the colonic mucosa were evaluated using immunohistochemistry, Western blotting, biochemical analyses or ELISA. Ten minutes before UC induction, drugs were microinjected into the relevant nuclei in rat brain to produce chemical stimulation or chemical lesion.Results: Microinjection of glutamate (3, 6 and 12 µg) into the PVN dose-dependently decreased the CDS in UC rats. This protective effect was eliminated after kainic acid (0.3 µg) was microinjected into PVN or into the nucleus tractus solitarius (NTS) that caused chemical lesion of these nuclei. This protective effect was also prevented when the AVP-V 1 receptor antagonist DPVDAV (200 ng) was microinjected into the NTS. The discharge frequency of the vagus was markedly decreased following microinjection of glutamate into the PVN. Microinjection of glutamate into the PVN in UC rats significantly increased the cell proliferation and anti-oxidant levels, and decreased the apoptosis and Bax and caspase 3 expression levels and reduced the pro-inflammatory factors in the colonic mucosa. Conclusion: The activation of hypothalamic PVN exerts protective effects against UC, which is mediated by the NTS and vagus. The effects may be achieved via anti-oxidative, anti-apoptotic, and anti-inflammatory factors.

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“…1 A recent study used a tagged single-nucleotide polymorphism (SNP) approach to characterize the variation in glioma-associated oncogene homolog 1 (GLI1) and tested for association with IBD in Scottish Caucasians. 2 Analysis of two tSNPs (rs2228224 and rs2228226) in this cohort demonstrated a significant association of GLI1 with both IBD and UC and a borderline association of GLI1 with CD, largely due to the non-synonymous rs22282260 (Q1100E), with the minor allele conferring susceptibility.…”

Section: Introductionmentioning

confidence: 99%

Evidence that glioma-associated oncogene homolog 1 is not a universal risk gene for inflammatory bowel disease in Caucasians

et al. 2010

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The transcription factor glioma-associated oncogene homolog 1 (GLI1) has a central function in gastrointestinal tract development and homeostasis. A non-synonymous single-nucleotide polymorphism (SNP) (rs2228226; Q1100E) in GLI1, which impairs GLI1 function in vitro, has been proposed as a risk factor for inflammatory bowel disease (IBD). In this study, we assessed the cumulative evidence for association of GLI1 with IBD. New genotype data for rs2228226 from New Zealand (907 controls, 990 IBD patients) and Belgian Caucasian case-control data sets (312 controls, 1214 IBD patients) were combined with data from the National Institute of Diabetes and Digestive and Kidney Diseases and three previously studied Caucasian case-control data sets. Meta-analysis of rs2228226 did not detect any association with ulcerative colitis (UC) (P ¼ 0.09, odds ratio (OR) ¼ 1.07, 95% confidence interval (CI) ¼ 0.92-1.24), Crohn's disease (CD) (P ¼ 0.29, OR ¼ 1.06, 95% CI ¼ 0.93-1.21) or overall IBD (P ¼ 0.15, OR ¼ 1.05, 95% CI ¼ 0.92-1.19). Our analyses of rs2228226 suggest that GLI1 is not a significant risk factor for IBD in Caucasians.

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Ulcerative colitis

Cited by 257 publications

References 137 publications

Haplotypes of PADI4 susceptible to rheumatoid arthritis are also associated with ulcerative colitis in the Japanese population

Haplotypes of PADI4 susceptible to rheumatoid arthritis are also associated with ulcerative colitis in the Japanese population

Glutamate microinjection into the hypothalamic paraventricular nucleus attenuates ulcerative colitis in rats

Evidence that glioma-associated oncogene homolog 1 is not a universal risk gene for inflammatory bowel disease in Caucasians

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