Increased nitric oxide production in collagenous and lymphocytic colitis

Lundberg, Jon O.; Herulf, Max; Olesen, Martin; Bohr, Johan; Tysk, Curt; Wiklund, Peter; Morcos, Edward; Hellström, Per M.; Weitzberg, Eddie; Järnerot, Gunnar

doi:10.1046/j.1365-2362.1997.2230757.x

Cited by 70 publications

(49 citation statements)

References 16 publications

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“…Colonic NO production is greatly increased in active MC caused by upregulation of inducible nitric oxide synthase (iNOS) in the colonic epithelium [66][67][68][69] . A major transcriptional inducer of iNOS gene expression is the transcription factor nuclear factor-κB (NF-κB).…”

Section: Nitric Oxide (No)mentioning

confidence: 99%

Diagnosis and management of microscopic colitis

Tysk¹,

Bohr²,

Nyhlin³

et al. 2008

WJG

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Microscopic colitis, comprising collagenous and lymphocytic colitis, is characterized clinically by chronic watery diarrhea, and a macroscopically normal colonic mucosa where diagnostic histopathological features are seen on microscopic examination. The annual incidence of each disorder is 4-6/100 000 inhabitants, with a peak incidence in 60-70-year-old individuals and a noticeable female predominance for collagenous colitis. The etiology is unknown. Chronic diarrhea, abdominal pain, weight loss, fatigue and fecal incontinence are common symptoms, which impair the health-related quality of life of the patient. There is an association with other autoimmune disorders such as celiac disease, diabetes mellitus, thyroid disorders and arthritis. Budesonide is the best-documented shortterm treatment, but the optimal long-term strategy needs further study. The long-term prognosis is good and the risk of complications including colonic cancer is low.

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Section: Nitric Oxide (No)mentioning

confidence: 99%

Diagnosis and management of microscopic colitis

Tysk¹,

Bohr²,

Nyhlin³

et al. 2008

WJG

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“…A novel minimally invasive technique for measurement of NO levels in the rectum has been developed. By this technique, increased rectal NO levels have been shown in patients with intestinal inflammatory disorders such as ulcerative colitis, Crohn's disease, collagenous colitis, and celiac disease (7,8,16,19). We have recently shown that rectal NO levels are greatly increased in patients with infectious gastroenteritis, including Clostridium difficile-associated diarrhea (CDAD) (9).…”

mentioning

confidence: 99%

Rectal Nitric Oxide Gas and Stool Cytokine Levels during the Course of Infectious Gastroenteritis

Enocksson

Lundberg

Weitzberg

et al. 2004

Clin Vaccine Immunol

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Nitric oxide (NO) is known to be an important inflammatory mediator with a potential role in gastrointestinal diseases. We prospectively studied the luminal NO levels in 51 patients with infectious gastroenteritis, 35 patients with nonenteric bacterial infections, and 11 healthy control subjects. The levels of proinflammatory cytokines were simultaneously measured in the stools of patients with gastroenteritis. Rectal gas was sampled with balloon catheters made of silicone and was analyzed for NO levels by chemiluminescence. The median rectal NO level was 2,450 ppb in the acute phase of gastroenteritis and gradually decreased to 225 ppb after 3 to 8 weeks, whereas the median NO values were 150 ppb in patients with nonenteric bacterial infections and 100 ppb in healthy control subjects. Patients with Salmonella, Shigella, and Campylobacter infections generally had more severe symptoms and a higher median NO level (17,250 ppb) than patients with Clostridium difficileassociated diarrhea (median NO value, 275 ppb). Interleukin-1␤ levels were elevated in 82% of the patients at disease onset and decreased during the convalescent phase. In contrast, gamma interferon was detected in only 16% of the patients and was predominantly collected in stool samples collected during the subacute and convalescent stages. Our data point to the possibility of using this easy, minimally invasive method for luminal NO measurement as a diagnostic tool, among others, to evaluate the degree of intestinal inflammation in patients with infectious gastroenteritis.

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“…A potential protective role of NO in human IBD is supported by the findings of higher colonic NO induction in patients with collagenous colitis, a process with scarce inflammatory infiltration and absence of mucosal damage, than in ulcerative colitis (Lundberg et al, 1997). Although ulcerative colitis and collagenous colitis are distinct disorders, with differing etiopathogenesis, the lower NO concentrations observed in active ulcerative colitis compared with collagenous colitis may reflect impaired compensatory NO production by iNOS, in a condition characterized by increased formation of oxidant radicals.…”

Section: Salas Et Almentioning

confidence: 95%

Nitric Oxide Supplementation Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice

Salas

Gironella

Salas

et al. 2002

Laboratory Investigation

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SUMMARY:Nitric oxide (NO) synthesis is up-regulated in inflammatory bowel disease. However, its role in the pathophysiology of this condition is controversial. The aims of this study were to assess whether nitric oxide administration ameliorates experimental colitis and to determine the possible mechanisms underlying its effects on intestinal inflammation. For this purpose, the NO donor diethylamine NONOate (DETA/NO; 0.01, 0.1, 1, 5, or 10 mg/kg/day), or the DETA moiety, was administered daily to mice with dextran sulfate sodium-induced colitis. Daily body weight and colonic pathologic alterations at Day 10 were determined. Leukocyte endothelial cell interactions in colonic venules were assessed with intravital microscopy, and expression of endothelial cell adhesion molecules was determined using radiolabeled antibodies. IL-12 and IFN-␥ production were measured in intestinal tissue. Colitis induced a significant loss of body weight, reduction of colon length, and increase in colon weight and myeloperoxidase activity. Administration of 1 mg/kg/day DETA/NO significantly attenuated these pathologic changes. The marked increase in leukocyte rolling and adhesion in colonic venules of colitic mice were significantly reduced by administration of 1 mg/kg/day DETA/NO. Development of colitis was associated with a marked increase in endothelial expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and P-selectin. Supplementation with NO significantly attenuated the up-regulation of endothelial intercellular adhesion molecule-1 and P-selectin, but not vascular cell adhesion molecule-1, in colonic tissue. NO abrogated the increase in IL-12 and IFN-␥ mRNA expression in the colon of colitic mice. The DETA moiety alone did not have any effect on any of the parameters studied. In conclusion, exogenous NO supplementation significantly ameliorates dextran sulfate sodium-induced colitis. This effect is related to a reduction in leukocyte recruitment and proinflammatory cytokine production. (Lab Invest 2002, 82:597-607).

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Increased nitric oxide production in collagenous and lymphocytic colitis

Cited by 70 publications

References 16 publications

Diagnosis and management of microscopic colitis

Diagnosis and management of microscopic colitis

Rectal Nitric Oxide Gas and Stool Cytokine Levels during the Course of Infectious Gastroenteritis

Nitric Oxide Supplementation Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice

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