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PubMed2006

Calprotectin and lactoferrin in the assessment of intestinal inflammation and organic disease.

BACKGROUND AND AIMS: Calprotectin and lactoferrin are specific neutrophil-derived proteins, which can be measured in the feces because they are released by cells in inflammatory conditions. We evaluated the efficacy of calprotectin and lactoferrin in detecting organic disease as assessed by colonoscopy. METHODS: The study comprised 144 patients undergoing colonoscopy for lower gastrointestinal symptoms (abdominal pain, altered bowel habits, and bloody stools) (67), or inflammatory bowel disease activity, or surveillance for dysplasia (77). A single stool sample was assayed for calprotectin and lactoferrin. The proportion of patients correctly diagnosed with each test and the relationship with endoscopic and histological findings were measured. RESULTS: Fecal excretion of calprotectin significantly correlated with the finding of colonic inflammation at endoscopy, both in ulcerative colitis and in Crohn's disease (p<0,001 and p<0,008, respectively), while lactoferrin excretion significantly correlated with histological inflammation (p=0.001 and p=0.009 respectively). Recommended cut-off values need to be adjusted in the inflammatory bowel disease group. Overall sensitivity, specificity, positive predictive value, and diagnostic efficacy were 78, 83, 86, and 80% for calprotectin and 80, 85, 87, and 81% for lactoferrin, respectively. CONCLUSIONS: Fecal calprotectin and lactoferrin appear to be equally recommendable as inflammatory disease markers in patients with lower gastrointestinal symptoms. Both tests are needed to accurately discriminate activity in inflammatory bowel disease patients.

Adolescent↗
PubMed2005

Effect of bacterial chemotactic peptides on intestinal inflammation in animal models of acute and chronic "relapsed" colitis.

It is known that bacterial chemotactic peptides such as formyl-methionyl-leucyl-phenylalanine (fMLP) exacerbate colitis during the acute phase, but the precise role of fMLP during chronic "relapse" is unknown. In this study we examined the effect of bacterial peptides in animal models of acute and chronic "relapsed" colitis. Different parameters were evaluated, such as tissue damage, myeloperoxidase activity, and mucosal function. In acute trinitrobenezene sulfonic acid colitis, fMLP had significant adverse effects on mucosal function and worsened several parameters. In contrast, in chronic "relapsed" colitis the ability of fMLP to exacerbate the inflammation was dependent on whether it was confined to the lumen of the colon. Bacterial peptides such as fMLP appear to play a different role in the acute phase of inflammation compared with the chronic phase, depending on the integrity of the mucosal barrier.

Acute Disease↗
PubMed1992

Tumour necrosis factor alpha in stool as a marker of intestinal inflammation.

Measurement of disease activity in patients with inflammatory bowel disease is difficult. The best available methods are complex and time consuming, but it may be possible to use tumour necrosis factor alpha (TNF alpha) concentration in stool as a marker of disease activity. We measured TNF alpha concentrations in stool samples from normal children, infants with diarrhoea, and children with inflammatory bowel disease in active and inactive phases of the disease. In 10 normal children and 14 children with diarrhoea, median stool TNF alpha concentrations were 58 and 45 pg/g stool, respectively. Compared with diarrhoeal controls, stool TNF alpha concentrations were significantly increased in children with active Crohn's disease (n = 13, median 994 pg/g, p less than 0.0002) and active ulcerative colitis (n = 4, range 276-5982 pg/g, p less than 0.003). In patients with inactive disease, either as a result of surgery or treatment with steroids, the concentration of stool TNF alpha fell to those of controls. Measurement of stool TNF alpha concentrations may provide a simple way to monitor disease activity in inflammatory bowel disease.

Adolescent↗
PubMed2001

Control of intestinal inflammation by regulatory T cells.

Transfer of CD4+ T cells to immune-deficient mice in the absence of the CD25+ subset leads to the development of colitis, indicating that regulatory cells capable of controlling a bacteria-driven inflammatory response are present in normal mice. Cells with this function are present in the thymus as well as in the periphery of germ-free mice, suggesting they may be reactive with self-antigen. These cells resemble CD4+CD25+ cells that inhibit organ-specific autoimmunity, suggesting that a similar subset of regulatory T cells may control responses to self and foreign antigens. Development of colitis is dependent on accumulation of activated CD134L+ dendritic cells (DC) in the mesenteric lymph nodes, which is inhibited by CD4+CD25+ cells, indicating that regulatory T cells may control DC activation in vivo. Whilst inhibition of T-cell activation in vitro by CD4+CD25+ cells does not involve interleukin-10 and transforming growth factor-beta, these cytokines are required for the suppression of colitis. It may be that control of responses that activate the innate immune system requires multiple mechanisms of immune suppression. Recently, we identified CD4+CD25+ cells with immune suppressive activity in the thymus and peripheral blood of humans, raising the possibility that dysfunction in this mechanism of immune regulation may be involved in the development of autoimmune and inflammatory diseases.

ADP-ribosyl Cyclase↗
PubMed2003

Review article: mitogen-activated protein kinases in chronic intestinal inflammation - targeting ancient pathways to treat modern diseases.

Conventional treatment of chronic inflammatory disorders, including inflammatory bowel diseases, employs broad-range anti-inflammatory drugs. In order to reduce the side-effects and increase the efficacy of treatment, several strategies have been developed in the last decade to interfere with intercellular and intracellular inflammatory signalling processes. The highly conserved mitogen-activated protein kinase pathways regulate most cellular processes, particularly defence mechanisms such as stress reactions and inflammation. In this review, we provide an overview of the current knowledge of the specificity and interconnection of mitogen-activated protein kinase pathways, their functions in the gut immune system and published and ongoing studies on the role of mitogen-activated protein kinases in inflammatory bowel disease. The development of mitogen-activated protein kinase inhibitors and their use for the therapy of inflammatory disorders is a paradigm of the successful bridging of the gap between basic research and clinical practice.

Acute Disease↗
PubMed1993

Phenotypically distinct subsets of CD4+ T cells induce or protect from chronic intestinal inflammation in C. B-17 scid mice.

CD4+ T cells in the mouse can be subdivided into two fractions based on the level of expression of the CD45RB determinant. Previous studies have shown that these subsets are functionally distinct. We have further characterized the properties of these subpopulations in vivo by injecting them into C. B-17 scid mice. The animals restored with the CD45RBhighCD4+ T cell population developed a lethal wasting disease with severe mononuclear cell infiltrates into the colon and elevated levels of IFN-gamma mRNA. In contrast, animals restored with the reciprocal CD45RBlow subset or with unfractionated CD4+ T cells did not develop the wasting or colitis. Importantly, the co-transfer of the CD45RBlow population with the CD45RBhigh population prevented the wasting disease and colitis. These data indicate that important regulatory interactions occur between the CD45RBhigh and CD45RBlowCD4+ T cell subsets and that disruption of this mechanism has fatal consequences.

Animals↗
PubMed1999

Tc-99m dextran: a new and sensitive general purpose scintigraphic agent for diagnosing intestinal inflammation.

PURPOSE: This feasibility study was undertaken to compare the sensitivity of Tc-99m dextran with that of Tc-99m human immunoglobulin G to diagnose ulcerative colitis, and to explore its possible role in disease follow-up. MATERIALS AND METHODS: Twenty-six patients with active disease and six patients in remission underwent serial Tc-99m dextran scanning for as long as 3 hours or more after injection. Eight of the patients with active disease also underwent Tc-99m human immunoglobulin G imaging. RESULTS: Twenty-four of 26 (92%) patients with active ulcerative colitis had a positive result of the Tc-99m dextran study, mainly within 1 hour. In comparison, Tc-99m human immunoglobulin G accumulated abnormally in four of eight (50%) patients and had a relatively poor target localization with high persisting background even after 6 hours. Four of the six patients in remission still had a positive result of the dextran scan, but the abnormal uptake was less than that in the patients with active disease. The disease has recurred already in one of these patients. A patient with pancolitis who was receiving steroid enema therapy had intense uptake of Tc-99m dextran in the ascending colon, probability because it was outside the range of the enema. CONCLUSIONS: Tc-99m dextran is a sensitive and cost-effective agent to diagnose ulcerative colitis, and it may have a role in disease follow-up.

Adult↗
PubMed2007

The role of altered microbial signaling via mutant NODs in intestinal inflammation.

PURPOSE OF REVIEW: Recently, a new class of intracellular pattern recognition receptors belonging to the family of nucleotide binding and oligomerization domain (NOD)-like receptors that includes NOD1, NOD2 and IPAF has been described. These proteins are involved in recognizing bacterial components or their degradation constituents that are delivered within the cytoplasm. In this review we will analyze the role of NOD proteins in regulating immune homeostasis. RECENT FINDINGS: After an initial description of advances in our understanding of the function of these proteins, this review will focus on the contradictory finding that even though mutations in NOD2 proteins lead to a loss of function phenotype, the outcome is an increased inflammatory response. Different hypotheses to reconcile this observation will be proposed. SUMMARY: The cellular and tissue distribution of NOD molecules as well as their role in regulating inflammatory cytokine release renders these proteins particularly important in controlling the development of inflammatory reactions. This is confirmed by the discovery that mutations in the genes that code for NOD1 and NOD2 confer increased susceptibility to inflammatory bowel disease. We will discuss NOD2 involvement in the development of Crohn's disease.

Animals↗