Riccardo Troncone

Asl Caserta Campania Region, San Felice a Cancello, Campania, Italy

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Publications (395)1697.3 Total impact

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    ABSTRACT: Background: The European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) recommended in 2008, based on observational data, to avoid both early (less than 4 months) and late (7 or more months) introduction of gluten and to introduce gluten while the infant is still being breastfed. New evidence prompted ESPGHAN to revise these recommendations. Objective: To provide updated recommendations regarding gluten introduction in infants and the risk of developing coeliac disease (CD) during childhood. Summary: The risk of inducing CD through a gluten-containing diet exclusively applies to persons carrying at least one of the CD risk alleles. Since genetic risk alleles are generally not known in an infant at the time of solid food introduction, the following recommendations apply to all infants, although they are derived from studying families with first-degree relatives with CD. Although breastfeeding should be promoted for its other well-established health benefits, neither any breastfeeding nor breastfeeding during gluten introduction has been shown to reduce the risk of CD. Gluten may be introduced into the infant's diet anytime between 4-12 completed months of age. In children at high risk for CD, earlier introduction of gluten (4 vs. 6 mo or 6 vs. 12 mo) is associated with earlier development of CD autoimmunity (defined as positive serology) and CD, but the cumulative incidence of each in later childhood is similar. Based on observational data pointing to the association between the amount of gluten intake and risk of CD, consumption of large quantities of gluten should be avoided during the first weeks after gluten introduction and during infancy. However, the optimal amounts of gluten to be introduced at weaning have not been established.
    No preview · Article · Jan 2016 · Journal of Pediatric Gastroenterology and Nutrition
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    ABSTRACT: Objectives: Potential celiac disease (CD) patients are at an increased risk to developing CD as indicated by positive CD-associated serology. We investigated in duodenal mucosa of such patients the presence of both IL-21 and IL-17A and the role of gliadin peptides and IL-15 in their expression. Methods: Duodenal biopsies from 76 active CD, 90 potential CD, and 58 control patients were analyzed for IL-21 and/or IL-17A production by quantitative real-time PCR, immunohistochemistry, flow cytometry, and ELISA. The presence of IL-21 receptor was investigated by western blot. Potential CD duodenal fragments were cultured with gliadin peptides (PTG) and/or IL-15 and the expression/production of IL-21 and IL-17A assessed by quantitative real-time PCR and by immunohistochemistry. Results: In potential CD, IL-21 was lower than in active CD, in terms of RNA expression (P<0.01), density of lamina propria (LP) IL-21(+) cells (P<0.05), and protein secretion (P<0.05). Also, IL-21R was weakly detectable in potential CD. Several LP cell types produced IL-21 in CD. In potential CD, CD4(+)IL-21(+) cells increased after PMA-ionomycin stimulation and co-produced IFN-γ but not IL-17A. After 24 hours of culture stimulation with PTG, IL-21-producing cells increased but not the ones producing IL-17A. This increase was further enhanced by the addition of IL-15 to culture medium. Conclusions: In potential CD, IL-21 is less expressed than in active CD; however, IL-21-producing cells are present and prone to respond after specific stimuli. This suggests a key role of IL-21 in the progression of mucosal damage in CD.Am J Gastroenterol advance online publication, 12 January 2016; doi:10.1038/ajg.2015.390.
    No preview · Article · Jan 2016 · The American Journal of Gastroenterology
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    ABSTRACT: Celiac disease (CD) is a common lifelong food intolerance triggered by dietary gluten affecting 1% of the general population. Gliadin-specific T-cell lines and T-cell clones obtained from intestinal biopsies have provided great support in the investigation of immuno-pathogenesis of CD. In the early 2000 a new in vivo, less invasive, approach was established aimed to evaluate the adaptive gliadin-specific T-cell response in peripheral blood of celiac patients on a gluten free diet. In fact, it has been demonstrated that three days of ingestion of wheat-containing food induces the mobilization of memory T lymphocytes reactive against gliadin from gut-associated lymphoid tissue into peripheral blood of CD patients. Such antigen-specific T-cells releasing interferon-γ can be transiently detected by using the enzyme-linked immunospot (ELISPOT) assays or by flow cytometry tetramer technology. This paper discusses the suitability of this in vivo tool to investigate the repertoire of gluten pathogenic peptides, to support CD diagnosis, and to assess the efficacy of novel therapeutic strategies. A systematic review of all potential applications of short oral gluten challenge is provided.
    Full-text · Article · Dec 2015 · Nutrients
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    ABSTRACT: Different approaches have been used to study the pattern of cytokines in celiac disease (CD). Laser capture microdissection (LCM) is a powerful tool for the isolation of specific tissue compartments. We aimed to investigate the mucosal immune response that takes place in different intestinal compartments of CD patients, dissected by LCM, analyzing cytokine expression profile. Frozen section of jejunum was obtained from 15 untreated CD and 15 control. Surface epithelium and lamina propria compartment were isolated by LCM. RNA from each LCM sample was extracted and, after a retrotranscription step, messenger RNA levels for MxA, IL-15, TNF-α, IFN-γ, IL-17aα, IL-21, IL-10, and TGF-β were determined by quantitative reverse transcriptase-PCR. Increased gene expression levels of MxA, IL-15, TNF-α, IL-10, and TGF-β was observed in the surface epithelium of untreated CD with respect to control. Furthermore, all the cytokines investigated were upregulated in the lamina propria of untreated CD as compared to control. Within the untreated CD group the expression of IL-15 was higher, in the surface epithelium than in the lamina propria, whereas the expression levels of IL-17 and IL-21 were higher in the lamina propria than in the surface epithelium. Finally, high levels of IL-10 and TGF-bβ were detected in both compartments of untreated CD biopsies. In CD, surface epithelium and lamina propria compartments, play a prominent role in determining innate and adaptive immunity, respectively. Conversely, surface epithelium and lamina propria produce high levels of anti-inflammatory cytokines, suggesting that both compartments are involved in the immunoregulatory response.
    Full-text · Article · Nov 2015 · Molecular and Cellular Biochemistry

  • No preview · Article · Oct 2015
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    Marco Sarno · Valentina Discepolo · Riccardo Troncone · Renata Auricchio
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    ABSTRACT: Celiac Disease (CD) is an immune-mediated systemic disorder elicited by gluten and related prolamines in genetically susceptible individuals and it is the result of the interaction between genetic and environmental factors. Among genetic risk factors, the strongest association is with the HLA class II DQ region; nevertheless at least 39 non-HLA loci are associated with CD. Gluten is the main environmental trigger of the disease. In addition, infant feeding and weaning practices as well as timing of gluten introduction in the diet have been suggested to contribute to CD risk. Furthermore a role for infectious agents and microbiota composition in disease development has also been proposed. Aim of this short review is to discuss the current knowledge on both genetic and environmental risk factors for the development of CD; moreover we will provide a brief overview of the possible strategies that could be envisaged to prevent this condition, at least in the population at-risk.
    Preview · Article · Aug 2015 · Italian Journal of Pediatrics
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    Full-text · Dataset · Jun 2015
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    ABSTRACT: Background & aims: The mechanisms of tissue destruction during progression of celiac disease are poorly defined. It is not clear how tissue stress and adaptive immunity contribute to the activation of intraepithelial cytotoxic T cells and the development of villous atrophy. We analyzed epithelial cells and intraepithelial cytotoxic T cells in family members of patients with celiac disease, who were without any signs of adaptive antigluten immunity, and in potential celiac disease patients, who have antibodies against tissue transglutaminase 2 in the absence of villous atrophy. Methods: We collected blood and intestinal biopsy specimens from 268 patients at tertiary medical centers in the United States and Italy from 2004 to 2012. All subjects had normal small intestinal histology. Study groups included healthy individuals with no family history of celiac disease or antibodies against tissue transglutaminase 2 (controls), healthy family members of patients with celiac disease, and potential celiac disease patients. Intraepithelial cytotoxic T cells were isolated and levels of inhibitory and activating natural killer (NK) cells were measured by flow cytometry. Levels of heat shock protein (HSP) and interleukin 15 were measured by immunohistochemistry, and ultrastructural alterations in intestinal epithelial cells (IECs) were assessed by electron microscopy. Results: IECs from subjects with a family history of celiac disease, but not from subjects who already had immunity to gluten, expressed higher levels of HS27, HSP70, and interleukin-15 than controls; their IECs also had ultrastructural alterations. Intraepithelial cytotoxic T cells from relatives of patients with celiac disease expressed higher levels of activating NK receptors than cells from controls, although at lower levels than patients with active celiac disease, and without loss of inhibitory receptors for NK cells. Intraepithelial cytotoxic T cells from potential celiac disease patients failed to up-regulate activating NK receptors. Conclusions: A significant subset of healthy family members of patients with celiac disease with normal intestinal architecture had epithelial alterations, detectable by immunohistochemistry and electron microscopy. The adaptive immune response to gluten appears to act in synergy with epithelial stress to allow intraepithelial cytotoxic T cells to kill epithelial cells and induce villous atrophy in patients with active celiac disease.
    Full-text · Article · May 2015 · Gastroenterology
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    ABSTRACT: The ancient diploid Triticum monococcum is of special interest as a candidate low-toxic wheat specie for celiac disease patients. Here, we investigated how an in vitro gastro-intestinal digestion, affected the immune toxic properties of gliadin from diploid compared to hexaploid wheat. Gliadins from Triticum monococcum, and Triticum aestivum cultivars were digested using either a partial proteolysis with pepsin-chymotrypsin, or an extensive degradation that used gastrointestinal enzymes including the brush border membrane enzymes. The immune stimulatory properties of the digested samples were investigated on T-cell lines and jejunal biopsies from celiac disease patients. The T-cell response profile to the Triticum monococcum gliadin was comparable to that obtained with Triticum aestivum gliadin after the partial pepsin-chymotrypsin digestion. In contrast, the extensive gastrointestinal hydrolysis drastically reduced the immune stimulatory properties of Triticum monococcum gliadin. Mass spectrometry-based analysis showed that several Triticum monococcum peptides, including known T-cell epitopes, were degraded during the gastrointestinal treatment, whereas many of Triticum aestivum gliadin survived the gastrointestinal digestion. The pattern of Triticum monococcum gliadin proteins is sufficiently different from those of common hexaploid wheat to determine a lower toxicity in celiac disease patients following in vitro simulation of human digestion. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Full-text · Article · May 2015 · Molecular Nutrition & Food Research
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    ABSTRACT: Coeliac disease has for a long time simply been regarded as a gluten-dependent enteropathy and a duodenal biopsy was required in all patients for the diagnosis. It is now accepted that autoimmunity against transglutaminase 2 is an earlier, more universal and more specific feature of coeliac disease than histologic lesions. Moreover, high serum levels of combined anti-transglutaminase 2 and anti-endomysium antibody positivity have excellent predictive value for the presence of enteropathy with villous atrophy. This makes the histology evaluation of the gut no longer necessary in well defined symptomatic paediatric patients with compatible HLA-DQ2 and/or DQ8 background. The biopsy-sparing diagnostic route is not yet recommended by gastroenterologists for adults, and certain clinical circumstances (immunodeficiency conditions, extraintestinal manifestations, type-1 diabetes mellitus, age less than 2 years) may require modified diagnostic approaches. Coeliac patients with preserved duodenal villous structure do exist and these need a more extended evaluation by immunologic and molecular biology tools. Copyright © 2015 Elsevier Ltd. All rights reserved.
    No preview · Article · May 2015 · Baillière&#x027 s Best Practice and Research in Clinical Gastroenterology
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    ABSTRACT: Bifidobacteria have been reported to reduce inflammation and contribute to intestinal homeostasis. However, the interaction between these bacteria and the gut immune system remains largely unknown. Because of the central role played by dendritic cells (DCs) in immune responses, we examined in vitro the effects of a Bifidobacteria mixture (probiotic) on DC functionality from children with inflammatory bowel disease. DCs obtained from peripheral blood monocytes of patients with Crohn's disease (CD), ulcerative colitis, and noninflammatory bowel disease controls (HC) were incubated with fluorochrome-conjugated particles of Escherichia coli or DQ-Ovalbumin (DQ-OVA) after a pretreatment with the probiotic, to evaluate DC phenotype, antigen sampling and processing. Moreover, cell supernatants were collected to measure tumor necrosis factor alpha, interferon gamma, interleukin 17, and interleukin 10 production by enzyme-linked immunosorbent assay. DCs from CD children showed a higher bacteria particles uptake and DQ-OVA processing after incubation with the probiotic; in contrast, DC from both ulcerative colitis and HC showed no significant changes. Moreover, a marked tumor necrosis factor alpha release was observed in DC from CD after exposure to E. coli particles, whereas the probiotic did not affect the production of this proinflammatory cytokine. In conclusion, the Bifidobacteria significantly improved the antigen uptake and processing by DCs from patients with CD, which are known to present an impaired autophagic functionality, whereas, in DCs from ulcerative colitis and HC, no prominent effect of probiotic mixture was observed. This improvement of antigen sampling and processing could partially solve the impairment of intestinal innate immunity and reduce uncontrolled microorganism growth in the intestine of children with inflammatory bowel disease.
    No preview · Article · Apr 2015 · Inflammatory Bowel Diseases

  • No preview · Article · Apr 2015 · Gastroenterology
  • Riccardo Troncone · Marco Sarno

    No preview · Article · Apr 2015 · World review of nutrition and dietetics

  • No preview · Article · Apr 2015 · Gastroenterology
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    ABSTRACT: There exists a wide variation in the reported incidence of coeliac disease in recent decades. We aimed to evaluate the incidence rate of coeliac diagnoses performed in an Italian region, Campania, between 2011 and 2013 and its variation therein. All coeliac diagnoses made from 2011 to 2013 and registered within the Campania coeliac disease register (CeliacDB) were identified. Incidence rates were analysed by sex, age and province of residence, with a Poisson model fitted to determine incidence rate ratios. We found 2049 coeliac disease diagnoses registered in the CeliacDB between 2011 and 2013; 1441 of these patients were female (70.4%) and 1059 were aged less than 19 years (51.7%). The overall incidence of coeliac disease in Campania was 11.8 per 100,000 person-years (95% CI 11.3-12.3) during the study period, with marked variation by age [27.4 per 100,000 person-years (95% CI 25.8-29.1) in children under 19 years of age and 7.3 per 100,000 (95% CI 6.8-7.8) in adults] and sex [16.1 per 100,000 person-years in females (95% CI 15.3-16.9) and 7.2 per 100,000 person-years in males (95% CI 6.6-7.8)]. Coeliac disease incidence was roughly similar in Naples, Salerno, Caserta and Avellino, but about half in Benevento. More than 80% of our study population was diagnosed by the combination of positive antitransglutaminase IgA and Marsh 3. More than half of the patients were symptomatic at the time of coeliac disease diagnosis (39.7% had a classical presentation and 21.1% a non-classical one according to the Oslo definition). Coeliac disease incidence was roughly similar among Campania provinces, except in Benevento where it was about half, probably due to less awareness of coeliac disease in this area. The incidence of coeliac disease in Campania appears to be lower than that reported by most of the previous literature, suggesting the necessity of new coeliac awareness programmes.
    Full-text · Article · Apr 2015 · United European Gastroenterology Journal
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    ABSTRACT: Background New evidence emerged on early feeding practices and the risk of coeliac disease.AimTo systematically update evidence on these practices to find out whether there is a need to revise current recommendations.MethodsMEDLINE, EMBASE and the Cochrane Library were searched from July 2012 (end of last search) to February 2015 for studies of any design that assessed the effect of gluten consumption and breastfeeding on the development of coeliac disease and/or coeliac disease-related autoimmunity.ResultsWe identified 21 publications, including two, new, large, randomised controlled trials performed in high-risk infants. Exclusive or any breastfeeding, as well as breastfeeding at the time of gluten introduction, did not reduce the risk of developing coeliac disease during childhood. For infants at high risk of developing coeliac disease, gluten introduction at 4 months of age in very small amounts, or at 6 or 12 months of age, resulted in similar rates of coeliac disease diagnosis in early childhood. Later gluten introduction was associated with later development of coeliac specific autoimmunity and coeliac disease during childhood, but not total risk reduction. Observational studies indicate that consumption of a higher amount of gluten at weaning may increase the risk for coeliac disease development.Conclusions Infant feeding practices (breastfeeding, time of gluten introduction) have no effect on the risk of developing coeliac disease during childhood (at least at specific timeframes evaluated in the included studies), necessitating an update of current European recommendations.
    Full-text · Article · Mar 2015 · Alimentary Pharmacology & Therapeutics
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    ABSTRACT: Celiac disease (CD) represents a spectrum, which includes cases with minor histological abnormalities (potential CD). The aim of this work is to evaluate the contribution of immunohistochemical analysis of duodenal biopsies to the diagnosis of gluten-related minor enteropathy. Duodenal biopsies from 56 untreated CD patients and 56 controls were analyzed for CD3 and γδ intraepithelial lymphocytes number, γδ /CD3 ratio, density of CD25+ lamina propria cells. A discriminant equation was obtained by which 61 more biopsies with normal villous architecture were blindly evaluated. All the immunohistochemical parameters were significantly different between CD and control patients. None of the single parameters showed sufficient specificity for CD. The combination of all four markers resulted in the following discriminant equation: Dscore = (CD3 x 0.06) - (γδ x 0.119) + (CD25 x 0.012) + (γδ /CD3 x 0.131) - 4.709. Using this discriminant score patients were correctly classified as celiac or controls in 97.3% of cases. When this equation was applied to a validation set of 61 patients with normal villous architecture and unknown diagnosis, 92.9% of those with a positive score turned out to be potential celiac patients. However, a normal score did not exclude this condition. Immunohistochemistry represents a very specific tool for the diagnosis of CD, but does lack sensitivity in detecting all potential CD cases.
    No preview · Article · Dec 2014 · Journal of Pediatric Gastroenterology and Nutrition
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    Maria Vittoria Barone · Riccardo Troncone · Salvatore Auricchio
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    ABSTRACT: Celiac disease (CD) is a frequent inflammatory intestinal disease, with a genetic background, caused by gliadin-containing food. Undigested gliadin peptides induce innate and adaptive T cell-mediated immune responses. The major mediator of the stress and innate immune response to gliadin peptides (i.e., peptide 31-43, P31-43) is the cytokine interleukin-15 (IL-15). The role of epithelial growth factor (EGF) as a mediator of enterocyte proliferation and the innate immune response has been described. In this paper, we review the most recent literature on the mechanisms responsible for triggering the up-regulation of these mediators in CD by gliadin peptides. We will discuss the role of P31-43 in enterocyte proliferation, structural changes and the innate immune response in CD mucosa in cooperation with EGF and IL-15, and the mechanism of up-regulation of these mediators related to vesicular trafficking. We will also review the literature that focuses on constitutive alterations of the structure, signalling/proliferation and stress/innate immunity pathways of CD cells. Finally, we will discuss how these pathways can be triggered by gliadin peptide P31-43 in controls, mimicking the celiac cellular phenotype.
    Preview · Article · Nov 2014 · International Journal of Molecular Sciences
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    ABSTRACT: Although dietary counseling is generally recommended in children with food allergy (FA), its effect on the nutritional status of these patients has not yet been evaluated. Our nonrandomized multicenter prospective intervention study was undertaken to investigate the effects of dietary counseling on children with FA. Anthropometric data, dietary intakes, and laboratory biomarkers of nutritional status were evaluated in children with FA (aged 6 to 36 months) before and after dietary counseling, by multidisciplinary teams composed of pediatricians, dietitians, and nurses. Ninety-one children with FA (49 boys and 42 girls; mean age 18.9 months, 95% CI 16.5 to 21.3) were evaluated; 66 children without FA (41 boys and 25 girls; mean age 20.3 months, 95% CI 17.7 to 22.8) served as controls providing baseline values only. At enrollment, energy and protein intakes were lower in children with FA (91 kcal/kg/day, interquartile range [IQR]=15.1, minimum=55.2, maximum=130.6; and 2.2 g/kg/day, IQR=0.5, minimum=1.5, maximum=2.7, respectively) than in children without FA (96 kcal/kg/day, IQR=6.1, minimum=83.6, maximum=118.0; and 4.6 g/kg/day, IQR=1.2, minimum=2.0, maximum=6.1, respectively; P<0.001). A weight to length ratio <2 standard deviations was more frequent in children with FA than in children without FA (21% vs 3%; P<0.001). At 6 months following dietary counseling, the total energy intake of children with FA was similar to the baseline values of control children. Dietary counseling also resulted in a significant improvement of their anthropometric and laboratory biomarkers of nutritional status. The results of our study support the crucial role of dietary counseling in the clinical management of children with FA.
    Full-text · Article · Sep 2014 · Journal of the American Academy of Nutrition and Dietetics

  • No preview · Article · Sep 2014

Publication Stats

7k Citations
1,697.30 Total Impact Points


  • 2015
    • Asl Caserta Campania Region
      San Felice a Cancello, Campania, Italy
  • 1994-2015
    • University of Naples Federico II
      • • Department of Translational Medical Sciences
      • • Department of Molecular Medicine and Medical Biotechnology
      Napoli, Campania, Italy
  • 2004
    • Birmingham Children's Hospital NHS Foundation Trust
      • Department of Gastroenterology and Nutrition
      Birmingham, England, United Kingdom
  • 2002
    • Università degli Studi di Salerno
      Fisciano, Campania, Italy
    • American Society for Nutrition
      American Fork, Utah, United States
  • 2001
    • Universitätsklinikum Tübingen
      Tübingen, Baden-Württemberg, Germany
    • University of Hawaiʻi at Mānoa
      Honolulu, Hawaii, United States
    • Indiana University-Purdue University Indianapolis
      Indianapolis, Indiana, United States
  • 1999
    • Riley Hospital for Children
      Indianapolis, Indiana, United States
  • 1998
    • Shaare Zedek Medical Center
      • Department of Pediatrics
      Yerushalayim, Jerusalem, Israel
  • 1983-1998
    • Second University of Naples
      Caserta, Campania, Italy
  • 1992
    • The American University of Rome
      Roma, Latium, Italy
  • 1987-1991
    • The University of Edinburgh
      • Gastro-Intestinal Unit
      Edinburgh, Scotland, United Kingdom
  • 1988
    • Western General Hospital
      Edinburgh, Scotland, United Kingdom