Flow cytometric measurement of intracellular migration inhibition factor and tumour necrosis factor alpha in the mucosa of patients with coeliac disease

O’Keeffe, Joan; Lynch, Stephen Anthony; Whelan, A.; Jackson, J. F.; Kennedy, N. P.; Weir, Donald G.; Feighery, Conleth

doi:10.1046/j.1365-2249.2001.01594.x

Cited by 32 publications

(23 citation statements)

References 35 publications

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“…Theoretically, if serologic recovery precedes histologic recovery, then inclusion of subjects who had a follow-up biopsy very soon after diagnosis might underestimate test performance. There was 1 study of tTG 27 (237 patients) and 3 studies of EMA 22,34,39 (total 107 patients) which included any patients who had been on a GFD for less than 11 months. Based upon the mean/median GFD duration in these studies, the number of patients involved is small and unlikely to have meaningfully influenced our findings.…”

Section: Discussionmentioning

confidence: 99%

Tests for Serum Transglutaminase and Endomysial Antibodies Do Not Detect Most Patients With Celiac Disease and Persistent Villous Atrophy on Gluten-free Diets: a Meta-analysis

et al. 2017

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Background & Aims Tests to measure serum endomysial antibodies (EMA) and antibodies to tissue transglutaminase (tTG) were developed to screen for celiac disease in patients consuming gluten. However, they are commonly used to monitor patients on a gluten-free diet (GFD). We conducted a meta-analysis to assess the sensitivity and specificity of tTG IgA and EMA IgA assays in identifying patients with celiac disease who have persistent villous atrophy despite a GFD. Methods We searched PUBMED, EMBASE, BIOSIS, SCOPUS, clinicaltrials.gov, Science Citation Index, and Cochrane Library databases through November 2016. Inclusion criteria were studies of subjects with biopsy-confirmed celiac disease, follow-up biopsies and measurement of serum antibodies on a GFD, biopsy performed on subjects regardless of symptoms or antibody test results. Our analysis excluded subjects with refractory celiac disease, undergoing gluten challenge, or consuming a prescribed oats-containing GFD. Tests were considered to have positive or negative findings based on manufacturer cut-off values. Villous atrophy was defined as a Marsh 3 lesion or villous height:crypt depth ratio below 3.0. We constructed forest plots to determine the sensitivity and specificity of detection for individual studies. For the meta-analysis, a bivariate random effects model was used to jointly model sensitivity and specificity. Results Our search identified 5408 unique citations. Following review of abstracts, 442 articles were reviewed in detail. Only 26 studies (6 of tTG assays, 15 of EMA assays, and 5 of tTG and EMA assays) met our inclusion criteria. The most common reason studies were excluded from our analysis was inability to cross-tabulate histologic and serologic findings. The serum assays identified patients with persistent villous atrophy with high levels of specificity: 0.83 for the tTG IgA assay (95% CI, 0.79–0.87) and 0.91 for the EMA IgA assay (95% CI, 0.87–0.94). However, they detected villous atrophy with low levels of sensitivity: 0.50 for the tTG IgA assay (95% CI, 0.41–0.60) and 0.45 for the EMA IgA assay (95% CI, 0.34–0.57). The tests had similar levels of performance in pediatric and adult patients. Conclusions In a meta-analysis of patients with biopsy-confirmed celiac disease undergoing follow-up biopsy on a gluten-free diet, we found that tests for serum tTG IgA and EMA IgA levels had low sensitivity (below 50%) in detection of persistent villous atrophy. We need more-accurate non-invasive markers of mucosal damage in children and adults with celiac disease who are following a GFD.

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Section: Discussionmentioning

confidence: 99%

Tests for Serum Transglutaminase and Endomysial Antibodies Do Not Detect Most Patients With Celiac Disease and Persistent Villous Atrophy on Gluten-free Diets: a Meta-analysis

et al. 2017

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“…Therefore, epithelial cells are the first cells to contact with gliadin peptides and they can act as sentinels initiating the proinflammatory response. In this sense, increased intracellular levels of MIF have been found in epithelial cells of celiac patients compared with healthy controls (P ¼ 0.005 14 ). We aimed at testing the etiological role of this gene in celiac susceptibility through a case-control study with 531 Spanish celiac patients and 887 healthy controls of the same ethnic background.…”

Section: Introductionmentioning

confidence: 99%

Involvement of macrophage migration inhibitory factor gene in celiac disease susceptibility

et al. 2007

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The MIF gene has been associated with several diseases with inflammatory and autoimmune background, such as ulcerative colitis, rheumatoid arthritis and systemic lupus erythematosus. We aimed at testing the influence of two functional MIF promoter variants in celiac disease (CD) susceptibility. A (CAAT) 5-8 tetranucleotide repeat at position À794 and a singlenucleotide polymorphism at À173G/C were analyzed in the Spanish population (531 patients and 887 healthy controls). w 2 statistics or Fisher exact test were used for comparisons. The À173C allele significantly increased risk ((CC þ GC) vs GG: odds ratio (OR) (95% confidence interval (CI)) ¼ 1.41 (1.10-1.81); P ¼ 0.005), as did carriage of the (CAAT) 7 allele (OR (95% CI) ¼ 1.36 (1.02-1.82); P ¼ 0.03) and of the haplotype (CAAT) 7 //À173C (OR (95% CI) ¼ 1.33 (1.00-1.76); P ¼ 0.04). Our data evidence for first time the role of the MIF gene increasing predisposition to CD. A common effect of MIF variants seems to underlie the etiology of these complex conditions.

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“…Masser et al 40 observed the expression of MIF in human gastric, smallintestinal, and colonic epithelium by immunohistochemical analysis. O'Keeffe et al 41 demonstrated that MIF protein was constitutively expressed in intraepithelial lymphocytes, T cells, and epithelial cells in normal intestinal mucosa. In the mouse colon, we found that weak MIF-positive staining was observed in the epithelial cells and infiltrated mononuclear cells in the colonic mucosa.…”

Section: Mif Expression In Stomach Intestine Liver and Pancreasmentioning

confidence: 99%

“…60 Lo et al 61 reported that MIF was diffusely expressed in the entire thickness of the colon in patients with acute graft-versus-host disease (GVHD). In this disease, macrophages and T cells infiltrating the mucosa were confined to areas of strong MIF expression.…”

Section: Intestinal Inflammationmentioning

confidence: 99%

Pathophysiological roles of macrophage migration inhibitory factor in gastrointestinal, hepatic, and pancreatic disorders

et al. 2005

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Macrophage migration inhibitory factor (MIF) is a unique protein, participating in inflammation, immune response, and cell growth. MIF was first discovered as a lymphokine involved in delayed hypersensitivity and various macrophage functions, including phagocytosis, spreading, and tumoricidal activity. It has been reported that MIF is associated with the pathogenesis of a variety of diseases. MIF expression was increased at inflammatory sites in diseases such as rheumatoid arthritis and glomerulonephritis. In experimental inflammatory disease, blockade of MIF bioactivity inhibited the severity of disease activity. On the other hand, MIF expression is also increased in tumor lesions, and MIF plays a role as a cell growth factor. MIF has been reported to be constitutively expressed in gut, liver, and pancreas. In patients with gastritis, inflammatory bowel disease, hepatitis, and pancreatitis, MIF expression was remarkably increased in both the serum and the local lesions. Blockade of MIF bioactivity inhibited and prevented inflammation in experimental gastritis, colitis, hepatitis, and pancreatitis. On the other hand, MIF expression was higher than that in normal tissues in colonic carcinomas and hepatocellular carcinoma both in vivo and in vitro. Blockade of MIF bioactivity successfully inhibited tumor cell growth in vivo and in vitro. MIF plays important roles in the pathogenesis of gastrointestinal, hepatic, and pancreatic disorders.

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Flow cytometric measurement of intracellular migration inhibition factor and tumour necrosis factor alpha in the mucosa of patients with coeliac disease

Cited by 32 publications

References 35 publications

Tests for Serum Transglutaminase and Endomysial Antibodies Do Not Detect Most Patients With Celiac Disease and Persistent Villous Atrophy on Gluten-free Diets: a Meta-analysis

Tests for Serum Transglutaminase and Endomysial Antibodies Do Not Detect Most Patients With Celiac Disease and Persistent Villous Atrophy on Gluten-free Diets: a Meta-analysis

Involvement of macrophage migration inhibitory factor gene in celiac disease susceptibility

Pathophysiological roles of macrophage migration inhibitory factor in gastrointestinal, hepatic, and pancreatic disorders

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