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PubMed2002

Specificity of tissue transglutaminase explains cereal toxicity in celiac disease.

Celiac disease is caused by a selective lack of T cell tolerance for gluten. It is known that the enzyme tissue transglutaminase (tTG) is involved in the generation of T cell stimulatory gluten peptides through deamidation of glutamine, the most abundant amino acid in gluten. Only particular glutamine residues, however, are modified by tTG. Here we provide evidence that the spacing between glutamine and proline, the second most abundant amino acid in gluten, plays an essential role in the specificity of deamidation. On the basis of this, algorithms were designed and used to successfully predict novel T cell stimulatory peptides in gluten. Strikingly, these algorithms identified many similar peptides in the gluten-like hordeins from barley and secalins from rye but not in the avenins from oats. The avenins contain significantly lower percentages of proline residues, which offers a likely explanation for the lack of toxicity of oats. Thus, the unique amino acid composition of gluten and related proteins in barley and rye favors the generation of toxic T cell stimulatory gluten peptides by tTG. This provides a rationale for the observation that celiac disease patients are intolerant to these cereal proteins but not to other common food proteins.

Algorithms↗

PubMed1993

The diagnostic value of the gliadin antibody test in celiac disease in children: a prospective study.

Serum gliadin antibodies (IgA/IgG) were determined in 191 consecutive children (median age, 2.75 years; range, 0.33-15.5 years) admitted for a small-intestinal biopsy on suspicion of celiac disease. The test was a diffusion-in-gel enzyme-linked immunosorbent assay (DIG-ELISA). Of these 191, 14 (7.3%) appeared to have untreated celiac disease. Depending on the choice of cut-off value of the test (combined determination of IgA and IgG), the sensitivity was 86-100%, the specificity was 97-99%, and the positive/negative predictive values were 70-92% and 99-100%, respectively. No variation according to age was found. Gliadin antibodies were determined in 47 children who had well-treated celiac disease. Fourteen of these children were also investigated when challenged with gluten. Gliadin antibodies (IgA or IgG) decreased significantly in 13 of 13 cases when the patients shifted from a gluten-containing diet to a gluten-free one. During the gluten challenge, the IgG and IgA increased in 14 of 14 and 11 of 14 cases, respectively (two patients suffered from IgA deficiency). In eight patients who later appeared to be free of celiac disease, the gliadin antibodies were determined on gluten-free diet and during gluten challenge; no significant differences in gliadin antibodies were found. We conclude that this test is useful in selecting patients with symptoms suggesting celiac disease for a small-intestinal biopsy. The test seems to be of some value in monitoring the effects of a gluten-free diet and during gluten challenge.

Adolescent↗

PubMed1989

Immunological aspects of diagnosis of celiac sprue in children.

Serum anti-gluten (AGA) and anti-reticulin (ARA) antibodies were examined in children suffering from celiac sprue (CS); cellular hypersensitivity to gluten was tested and secretion of immunoglobulins and anti-gluten antibodies into the culture medium after 24-hour in vitro cultivation of jejunal mucosal biopsies was investigated with the aim to assess significance of these methods for CS diagnosis. Indirect immunofluorescence was used in ARA determination, ELISA method for AGA determination, cellular hypersensitivity was examined using the test of leucocyte migration inhibition (LMIT) with gluten. ARA were detected in 69% of children with untreated CS and in 28% of CS children who were on a gluten-free diet. ARA specificity was 100%. Statistically significant higher titres of IgG AGA and IgA AGA were proved in children with untreated CS as compared with the control group. IgA AGA were detected significantly more frequently than IgG AGA. No relationship between positive AGA and the degree of alteration of the jejunal mucosa was found. IgG AGA sensitivity in CS children with pathological findings on the jejunal mucosa was 52%, specificity being 95%. IgA AGA sensitivity was 82% with specificity 90%. After a parallel application of IgA AGA and ARA, sensitivity of the tests rose up to 95.5%, specificity being 90%. Examinations of ARA and AGA have a significant importance for laboratory tests used for screening children with pathological findings on the jejunal mucosa and for indication to jejunal biopsies. The above tests do not replace jejunal biopsy in CS diagnosis. They can be applied in monitoring children with CS during gluten challenge and in checking how the gluten-free diet is observed. Significantly higher stimulation of leucocyte migration in gluten environment was proved in children suffering from CS as compared with the control group. Stimulation of migration is supposed to indicate cellular hypersensitivity to the antigen used in CS children. After a 24-hour culturing of jejunal mucosal biopsies, significantly elevated concentrations of IgA immunoglobulin and IgG, IgA and IgM AGA were found in the culture medium as compared with those obtained from cultured jejunal mucosal biopsies of control group children. The test of leucocyte migration inhibition and in vitro culturing of jejunal mucosa are quite complex and exacting methods when used in routine practice. Their significance lies in the fact they enable us to study in vitro immunological reactions in children suffering from celiac sprue.

Antibodies↗

PubMed1987

Dietary management of dermatitis herpetiformis.

Dermatitis herpetiformis (DH) is an extremely itchy, papulovesicular skin disease characterized in part by the presence of IgA at the dermal-epidermal junction. Eighty-five percent to 90% of DH patients have granular deposits of IgA at the dermal-epidermal junction, and essentially all of these patients have an associated, for the most part asymptomatic, gluten-sensitive enteropathy (GSE). The association of GSE and DH suggested that the cutaneous manifestations of DH could be controlled by the use of a gluten-free diet. Institution of a gluten-free diet in patients with DH and granular IgA deposits has been shown to be effective in controlling the cutaneous eruption of DH. Seventy percent to 100% of patients who begin a strict gluten-free diet have been shown to be able to decrease the dosage of medication needed to control their DH after a mean of eight to 18 months on the diet. Furthermore, 40% to 70% of patients with DH can control their skin disease completely, without any medication, after longer periods of time on the gluten-free diet (two years and longer). Although the gluten-free diet has been shown to be of great benefit in the control of the skin manifestations of DH, at the present time there is no evidence to suggest that the gluten-free diet is in any way protective against the risk of intestinal lymphoma that has been documented in GSE. Evaluation of the cutaneous IgA deposits in DH skin after long periods of time on a gluten-free diet suggests that there may be a slight decrease in the intensity of the IgA deposits, but the true pathogenetic relationship between the cutaneous IgA deposits, the cutaneous manifestations of DH, and the associated GSE remains unknown.

Celiac Disease↗

PubMed1986

Serum IgG subclass antibodies to gliadin and other dietary antigens in children with coeliac disease.

IgG subclasses of antibodies to the dietary antigens gliadin, glycgli (a gluten component), ovalbumin (OA) and beta-lactoglobulin (BLG) were quantified in children with coeliac disease (CD), nine on a gluten-containing diet, 15 on a gluten-free diet, and in appropriate controls. In addition, total serum IgG subclasses were measured. IgG1 and IgG3 antibodies to gluten and glycgli were detected in 9/9 and 8/9 CD-patient on a gluten-containing diet, respectively, and in 4/15 and 6/15 patients on a gluten-free diet. None of the controls had appreciable levels of IgG1 antibodies and only 1/22 of the controls had IgG3 antibodies to gliadin and glycgli. IgG2 and IgG4 antibodies to the same antigens were found in a few coeliacs and controls. Consecutive samples from coeliac children (8 patients) showed a clear relation between the exposure to gluten and a rise in IgG1 (8/8) and IgG3 antibody levels (7/8). In contrast, IgG antibodies to OA and BLG were almost exclusively of the IgG1 and IgG4 subclasses. The highest levels were found in children with CD, but the differences between the groups were not significant. Total serum IgG subclasses did not differ between the groups, but the IgG2 and IgG4 levels in most coeliac children were low. The production of IgG1 and IgG3 antibodies to gluten components may be an important precondition for the development of coeliac disease in susceptible individuals.

Adolescent↗

PubMed2000

Molecular basis of celiac disease.

Celiac disease (CD) is an intestinal disorder with multifactorial etiology. HLA and non-HLA genes together with gluten and possibly additional environmental factors are involved in disease development. Evidence suggests that CD4(+) T cells are central in controlling an immune response to gluten that causes the immunopathology, but the actual mechanisms responsible for the tissue damage are as yet only partly characterized. CD provides a good model for HLA-associated diseases, and insight into the mechanism of this disease may well shed light on oral tolerance in humans. The primary HLA association in the majority of CD patients is with DQ2 and in the minority of patients with DQ8. Gluten-reactive T cells can be isolated from small intestinal biopsies of celiac patients but not of non-celiac controls. DQ2 or DQ8, but not other HLA molecules carried by patients, are the predominant restriction elements for these T cells. Lesion-derived T cells predominantly recognize deamidated gluten peptides. A number of distinct T cell epitopes within gluten exist. DQ2 and DQ8 bind the epitopes so that the glutamic acid residues created by deamidation are accommodated in pockets that have a preference for negatively charged side chains. Evidence indicates that deamidation in vivo is mediated by the enzyme tissue transglutaminase (tTG). Notably, tTG can also cross-link glutamine residues of peptides to lysine residues in other proteins including tTG itself. This may result in the formation of complexes of gluten-tTG. These complexes may permit gluten-reactive T cells to provide help to tTG-specific B cells by a mechanism of intramolecular help, thereby explaining the occurrence of gluten-dependent tTG autoantibodies that is a characteristic feature of active CD.

Animals↗

PubMed2000

Does breast-feeding affect the risk for coeliac disease?

Coeliac disease, or permanent gluten sensitive enteropathy, has emerged as a widespread health problem. It is considered an immunological disease, possibly of autoimmune type, albeit strictly dependent on the presence in the diet of wheat gluten and similar proteins from rye and barley. There are reasons to believe that the aetiology of coeliac disease is multifactorial, i.e. that other environmental exposures than the mere presence in the diet of gluten affect the disease process. Our studies have shown that prolonged breast-feeding, or perhaps even more important, ongoing breast-feeding during the period when gluten-containing foods are introduced into the diet, reduce the risk for coeliac disease. The amount of gluten consumed is also of importance in as much as larger amounts of gluten-containing foods increase the risk for coeliac disease, while it still is uncertain if the age for introducing gluten into the diet of infants is important. Thus, a challenging possibility, that need to be further explored, is if the coeliac enteropathy can be postponed, or possibly even prevented for the entire life span, by favourable dietary habits early in life.

Age Factors↗

PubMed1995

Coeliac disease in childhood.

Coeliac disease usually presents in infancy or early childhood with diarrhoea, vomiting and interference with weight gain and growth. Withdrawal of dietary gluten is followed by resolution of the symptoms and signs and restoration of normal weight gain and growth; the characteristic subtotal villous atrophy of the jejunal mucosa also recovers. Later re-introduction of dietary gluten will lead to a return of the jejunal mucosal abnormality in the majority and to clinical relapse in many but not all. The severity and timing of both are variable and 5% of children initially considered on clinical, biopsy and gluten response evidence to have coeliac disease appear to develop permanent tolerance to gluten, although mucosal relapse may occur years after the re-introduction of dietary gluten in a minority, emphasizing the need for long-term follow-up. Although a diagnostic and subsequent follow-up jejunal biopsy are necessary to confirm the diagnosis, anti-gliadin IgA and IgG, anti-reticulum and anti-endomysium antibodies are now almost totally reliable in identifying children who have coeliac disease and are valuable in monitoring the adequacy of gluten withdrawal. Dietary compliance is frequently poor and regular supervision by a paediatric dietitian is needed; indeed, lifelong supervision to ensure gluten withdrawal is essential to reduce the chance of developing later gastrointestinal malignancy.

Adolescent↗

PubMed2006

Sourdough lactobacilli and celiac disease.

Celiac disease (CD) is one of the most common food intolerance. The only effective treatment for CD is a strict adherence to a gluten-free diet throughout the patient's lifetime. Gluten-free products are not widely available and are usually more expensive than their gluten-containing counterparts. There is, therefore, an urgent need to develop safe and effective therapeutic alternatives, to develop high-quality gluten-free products and to investigate the potential of the bread making biotechnology following ancient protocols which include long-time fermentation by selected sourdough lactic acid bacteria. This review describes the most relevant results related to biotechnologies that use selected sourdough lactic acid bacteria and probiotics as starters for sourdough fermentation to investigate their potential to decrease the risk of gluten contamination in gluten-free products. As shown by studies in vitro on celiac intestinal tissue and in vivo on CD patients, the bacterial proteolytic activity is rather promising not only as currently demonstrated for eliminating traces of contaminant gluten but probably also in perspective for the manufacture of tolerated baked goods.

Bread↗

PubMed2006

Celiac disease--sandwiched between innate and adaptive immunity.

Celiac disease (CD) patients are intolerant to gluten, proteins in wheat, and related cereals. Virtually all patients are human leukocyte antigen (HLA)-DQ2 or HLA-DQ8 positive and several studies have demonstrated that CD4 T cells specific for (modified) gluten peptides bound to these HLA-DQ molecules are found in patients but not in control subjects. These T cell responses are therefore thought to be responsible for disease development. Many immunogenic gluten peptides which may relate to the disease-inducing properties of gluten have now been identified. In addition, gluten can stimulate IL-15 production that ultimately leads to NKG2D-mediated epithelial cell killing. However, CD develops in only a minority of HLA-DQ2 and HLA-DQ8 individuals. This may be attributed to the default setting of the intestinal immune system: induction and maintenance of tolerance to dietary components and commensal flora. Although at present it is unknown why tolerance in CD is not established or broken, both environmental and genetic factors have been implicated. There is strong evidence for the existence of genes or gene variants on chromosomes 5, 6, and 19 that predispose to CD. In addition, type I interferons have been implicated in development of several autoimmune disorders, including CD. Thus, viral infection and/or tissue damage in the intestine may cause inflammation and induce protective Th1-mediated immunity leading to loss of tolerance for gluten. Once tolerance is broken, a broad gluten-reactive T cell repertoire may develop through determinant spreading. This may be a critical step toward full-blown disease.

Antigen-Presenting Cells↗

PubMed2003

Clarification of Muscat musts using wheat proteins and the flotation technique.

The bovine spongiform encephalopathy (BSE, mad cow) crisis has led some wine-makers to question gelatin as a fining agent and to reject the use of these animal proteins. The search for a substitute for gelatin was begun by comparing vegetable proteins (particularly gluten) with gelatin fining treatments. Clairette de Die (French-controlled appellation) is a sparkling sweet wine. The alcoholic fermentation begins in a tank, continues in a crown-cap bottle, and stops before the complete consumption of sugar. All particles present in the bottle have to be removed before corking, and it is important to have a must as clear as possible. This study concerned the clarifying of a Muscat must, treated with pectinases, using a very efficient flotation technique. The must is fined with bentonite/silica/protein (fish gelatin, wheat gluten, or lupin isolate) to induce flocculation and then pressurized (6 bar). After depressurization, microbubbles cling to flocculates and climb to the top of the flotation tank (this flotation foam is clarified using a rotary filter). At laboratory scale, gluten (20 g/hL) and gelatin (10 g/hL) (each combined with bentonite and silica gel) gave turbidities of 50 and 35 NTU, respectively (6.5 and 4.1% of that of the nontreated must). The Muscat must was also clarified by static settling. The turbidity decreased by 86% for the gluten/bentonite fining and by 60% for the gelatin/bentonite fining. Visually, gluten flocculation takes longer to occur and flocculates sedimentation is longer than with gelati, but the removal of insoluble particles is more complete and leads to lower turbidities. At an industrial scale, gluten (20 g/hL) and gelatin (10 g/hL) (each combined with bentonite and silica gel) gave turbidities of 60 and 48 NTU, respectively. Turbidities measured in the tanks 14 h after the flotation showed a better efficiency for the wheat gluten (24 NTU) compared to gelatin (28 NTU). This is explained by the static settling that completed the clarifying effect of the flotation. The last experiment showed comparable efficiencies for wheat gluten and lupin proteins. BSE caused a situation of crisis (in Europe particularly) leading the public and wine-makers to lose their confidence in the use of gelatin as fining agent and to reject animal proteins in general. It is proposed here that vegetable proteins could efficiently replace gelatin.

Bentonite↗

PubMed2005

Dietary guidelines and implementation for celiac disease.

Medical nutrition therapy is the only accepted treatment for celiac disease. This paper summarizes a review of scientific studies using the gluten-free diet, nutritional risk factors, controversial elements of the diet, and its implementation in treating celiac disease. Treatment for celiac disease requires elimination of the storage proteins found in wheat, rye, and barley. The inclusion of oats and wheat starch is controversial. Research supports that oats may be acceptable for patients with celiac disease and can improve the nutritional quality of the diet. However, use of oats is not widely recommended in the United States because of concerns of potential contamination of commercial oats. Studies assessing the contamination of commercial oats are limited. Research indicates no differences in patients choosing a strict wheat starch-containing, gluten-free diet vs. a naturally gluten-free diet. Factors other than trace gluten may be the cause of continued villous atrophy in some patients. The impact of nutrient malabsorption caused from untreated celiac disease is well documented. The diet and gluten-free products are often low in B vitamins, calcium, vitamin D, iron, zinc, magnesium, and fiber. Few gluten-free products are enriched or fortified, adding to the risk of nutrient deficiencies. Patients newly diagnosed or inadequately treated have low bone mineral density, imbalanced macronutrients, low fiber intake, and micronutrient deficiencies. Also troubling is the increased incidence of obesity seen in persons with celiac disease following a gluten-free diet. Because of the nutritional risks associated with celiac disease, a registered dietitian must be part of the health care team that monitors the patient's nutritional status and compliance on a regular basis.

Celiac Disease↗

PubMed2006

[Treatment and management of celiac disease].

In most patients the clinical course of celiac disease is unproblematic after the diagnosis has been made and a strict gluten-free diet is established. However, in rare cases complications like refractory sprue or lymphoma can occur. Individual management is required since the clinical presentation of celiac disease can be very heterogeneous. For example, it is a matter of controversy if asymptomatic patients, who have the same typical histological changes in their small bowel like patients with symptomatic celiac disease, should adhere to a gluten-free diet. A major problem is the compliance and the unintentional intake of gluten. A 100 % gluten-free diet is not possible since most food components are contaminated with trace amounts of gluten. Fortunately most patients tolerate these contaminations. Furthermore, the threshold for gluten contamination can differ highly among patients. One central point in patient care is the monitoring of a gluten-free diet and the timely recognition of complications. Therefore, the role of antibodies and duodenal histology in monitoring the course of the disease will be discussed.

Celiac Disease↗

PubMed2000

Endomysium antibodies are superior to gliadin antibodies in screening for coeliac disease in patients presenting supposed functional gastrointestinal symptoms.

OBJECTIVE: To study the accuracy of IgA- and IgC-gluten antibodies and endomysium antibodies as screening tools for endoscopy with small bowel biopsy for histologic diagnosing of coeliac disease. DESIGN: Comparing serology with histologic examination--the "gold standard" for diagnosing coeliac disease. SETTINGS: 1. The municipality of Osthammar, Sweden. 2. The catchment area of the University Hospital, Uppsala, Sweden. PATIENTS: 1. A random subsample (50 with dyspepsia, 50 with irritable bowel syndrome and 50 symptomless) of a representative sample from an adult Swedish general population (20-80 years; n = 1260). 2. All patients with a diagnosis of coeliac disease admitted to the University Hospital in Uppsala, Sweden during the course of 10 months. MAIN OUTCOME MEASURES: The accuracy of IgA- and IgG-gluten antibodies and endomysium antibodies. RESULTS: There were no significant correlations between IgA-gluten antibodies and IgG-gluten antibodies, on the one hand, and symptoms or symptom severity, on the other. Using duodenal biopsy results as the gold standard, IgA-gluten antibodies had a low specificity and IgG-gluten antibodies a low sensitivity, whereas endomysium antibodies had an excellent accuracy. CONCLUSION: Endomysium antibodies seem to be the screening test of choice. The load of diagnostic upper endoscopies would be considerably decreased compared to using gluten antibodies.

Adult↗

PubMed2002

Breast-feeding protects against celiac disease.

BACKGROUND: Celiac disease, or permanent gluten-sensitive enteropathy, is an immunologic disease strictly dependent on exposure to wheat gluten or related proteins in rye and barley. OBJECTIVE: The aim of this study was to explore whether breast-feeding and the mode of introducing dietary gluten influence the risk of celiac disease in childhood. DESIGN: A population-based incident case-referent study of Swedish children, 627 cases with celiac disease and 1254 referents, was conducted; 78% of the matched sets were included in the final analyses. A questionnaire was used to assess patterns of food introduction to infants. Models were built, based on current epidemiologic and immunologic knowledge of celiac disease, to study the potential influence of dietary patterns on disease risk and were evaluated by conditional logistic regression in multivariate analyses. RESULTS: The risk of celiac disease was reduced in children aged <2 y if they were still being breast-fed when dietary gluten was introduced [adjusted odds ratio (OR): 0.59; 95% CI: 0.42, 0.83]. This effect was even more pronounced in infants who continued to be breast-fed after dietary gluten was introduced (OR: 0.36; 95% CI: 0.26, 0.51). The risk was greater when gluten was introduced in the diet in large amounts (OR: 1.5; 95% CI: 1.1, 2.1) than when introduced in small or medium amounts. In older children, these risk factors were of no or only minor importance. CONCLUSIONS: The gradual introduction of gluten-containing foods into the diet of infants while they are still being breast-fed reduces the risk of celiac disease in early childhood and probably also during the subsequent childhood period.

Adolescent↗

PubMed1990

Beta 2-microglobulin levels in celiac disease.

The serum levels of beta 2-microglobulins (beta 2-m) were studied in 65 celiac children. Significant statistical differences (p less than 0.05) were found between the values of patients on a gluten-containing diet (mean +/- SD, 1.92 +/- 0.64 mg/L) and those on a gluten-free diet for less than (mean +/- SD, 2.38 +/- 0.76 mg/L) or greater than (mean +/- SD, 1.46 +/- 0.77 mg/L) 8 months. A significant difference was also found between the first group and the 15-subject control group, who underwent intestinal biopsy for low stature or chronic diarrhea but had normal intestinal mucosa (mean +/- SD, 1.56 +/- 0.42 mg/L). Serum beta 2-m levels were above normal values (less than 2 mg/L) in 10 of 26 (38.5%) celiac patients on a gluten-containing diet and in two of 15 (13.3%) subjects of the control group. The beta 2-m values of patients on a gluten-free diet for less than or equal to 8 months were significantly different (p less than 0.001) from those of patients on a gluten-free diet for greater than 8 months, as well from those of the control group. No significant differences were found between patients on a gluten-free diet for greater than 8 months and the control group. A significant correlation between the antigliadin antibody (AGA) IgA and beta 2-m in the patients on a gluten-free diet for greater than 8 months and control-group patients was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Celiac Disease↗

PubMed1981

Splenic atrophy in adult coeliac disease: is it reversible?

A study of splenic function in 28 patients with adult coeliac disease showed no significant correlation between the half life of heat-damaged red cells and either the duration of pre-treatment exposure to gluten or the length of time on a gluten free diet. A significant correlation was found between splenic size and duration of treatment; those patients who had been taking a gluten free diet for the longest time had the smallest spleens. Blood films from 11 of these 28 patients taken before treatment with a gluten free diet were compared with those taken between two and 15 years after the start of treatment. There was no tendency for the hyposplenic changes to regress. In the majority, the changes became more prominent despite strict adherence to the gluten free diet. These findings suggest that splenic atrophy in adult coeliac disease is not reversed by treatment with a gluten free diet and is unlikely to be related to the state of the jejunal mucosa or the duration of initial exposure to gluten.

Adolescent↗

PubMed1981

Labelling indices after 3H-thymidine incorporation during organ culture of duodenal mucosa in coeliac disease.

Incorporation of 3H-thymidine during organ culture of duodenal biopsy specimens from 34 coeliac and 10 non-coeliac patients was studied by autoradiography. High labelling indices were found in flat, coeliac mucosas. Gluten fractions, which provoked histological deterioration during culture, induced labelling of a greater proportion of crypt cells and higher migration rate than parallelly cultured specimens on gluten-free medium. No influences on crypt cell kinetics could be observed after culture with gluten fractions incapable of producing histological damage or with alpha-lactalbumin. In coeliac remission mucosas, labelling indices were at the same level as in non-coeliac biopsies, and no significant effects of gluten were observed. Autoradiography seems to be a fairly sensitive and reliable determinant of gluten toxicity by organ culture in coeliac disease and should supplement the histological appraisal of the biopsies. The increment of labelling indices provoked by gluten exposure seemed not merely to be a consequence of increased desquamation of cells from the biopsy surface but could imply a direct influence of gluten on crypt cell kinetics in coeliac disease.

Adolescent↗