Gastroenterology
Volume 136, Issue 3 , Pages 739-740, March 2009

Second Annual William K. Warren, Jr Prize for Excellence in Celiac Disease Research Awarded to Professor Salvatore Auricchio of Naples, Italy

published online 23 January 2009.

Richard Peek and K. Rajender Reddy, Section Editors

Article Outline

 

Professor Salvatore Auricchio, Professor of Pediatrics, University “Federico II” of Naples, was awarded the distinguished Warren Prize for 2008 and delivered the Warren Prize lecture at the University of California, San Diego. The Warren Prize was established by William K. Warren, Jr, and The William K. Warren Foundation to recognize investigators from the international scientific community whose research is judged to have made a significant contribution to celiac disease research. The award is presented at the annual research symposium sponsored by the William K. Warren Medical Research Center for Celiac Disease at the University of California, San Diego. Professor Auricchio was selected as this year's recipient by a group of scientific experts based on important contributions to celiac disease research by his group that span a 30-year period. Using epidemiologic approaches, his early studies showed a protective effect of breast feeding on the development of celiac disease.1 Further studies from his group revealed an increased occurrence of celiac disease in families, and discovered that families of celiac disease probands often have other affected members with celiac disease who are asymptomatic.

Professor Auricchio (Figure), in studies dating back almost 20 years, was among the first to draw attention to gliadin being an optimal substrate for the enzyme tissue transglutaminase and the possibility that interfering with enzyme activity might be used as a therapeutic approach.2, 3 His studies in collaboration with Dr Donald Kasarda explored the mechanisms by which gliadin peptides damage the small intestinal mucosa4 with a subsequent focus on class I restricted cytotoxic CD8+ T cells5, 6 and T cells that mediate regulatory functions.7 Early on, Professor Auricchio's group recognized the importance of innate immunity in the pathogenesis of celiac disease and that gliadin peptides, which differ from those thought to bind to DQ2 or DQ8, play a key role in activating innate immunity in the small intestinal mucosa.8, 9 Notably, his group, working together with Marco Londei, recognized the importance of the cytokine interleukin-15 in early gliadin-triggered events.10, 11, 12

In summary, Professor Auricchio's early application of epidemiologic approaches, together with the development of in vitro and translational models to increase our comprehension of the interactions between gliadin and the intestinal mucosa, laid important groundwork and led to greater understanding of the pathogenesis of celiac disease.

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References 

  1. Greco L, Mayer M, Grimaldi M, et al. The effect of early feeding on the onset of symptoms in celiac disease. J Pediatr Gastroenterol Nutr. 1985;4:52–55
  2. Porta R, Gentile V, Esposito C, et al. Cereal dietary proteins with sites for cross-linking by transglutaminase. Phytochemistry. 1990;29:2801–2804
  3. Auricchio S, De Ritis G, De Vincenzi M, et al. Amines protect in vitro the celiac small intestine from the damaging activity of gliadin peptides. Gastroenterology. 1990;99:1668–1674
  4. De Ritis G, Auricchio S, Jones HW, et al. In vitro (organ culture) studies of the toxicity of specific A-gliadin peptides in celiac disease. Gastroenterology. 1988;94:41–49
  5. Mazzarella G, Stefanile R, Camarca A, et al. Gliadin activates HLA class-I restricted CD8+ cells in celiac disease intestinal mucosa and induces the enterocyte apoptosis. Gastroenterology. 2008;134:1017–1027
  6. Gianfrani C, Troncone R, Mugione P, et al. Celiac disease association with CD8+ T cell response: identification of a novel gliadin-derived HLA-A2-restricted epitope. J Immunol. 2003;170:2719–2726
  7. Gianfrani C, Levings MK, Sartirana C, et al. Gliadin specific type-1 regulatory T cells from the intestinal mucosa of treated celiac patients inhibit pathogenic T cells. J Immunol. 2006;177:4178–4186
  8. Maiuri L, Picarelli A, Boirivant M, et al. Definition of the initial immunologic modifications upon in vitro gliadin challenge in the small intestine of celiac patients. Gastroenterology. 1996;110:1368–1378
  9. Maiuri L, Troncone R, Mayer M, et al. In vitro activities of A-gliadin-related synthetic peptides: damaging effect on the atrophic coeliac mucosa and activation of mucosal immune response in the treated coeliac mucosa. Scand J Gastroenterol. 1996;31:247–253
  10. Maiuri L, Ciacci C, Auricchio S, et al. Interleukin 15 mediates epithelial changes in celiac disease. Gastroenterology. 2000;119:996–1006
  11. Maiuri L, Ciacci C, Vacca L, et al. IL-15 drives the specific migration of CD94+ and TCR-gammadelta+ intraepithelial lymphocytes in organ cultures of treated celiac patients. Am J Gastroenterol. 2001;96:150–156
  12. Maiuri L, Ciacci C, Ricciardelli I, et al. Association between innate response to gliadin and activation of pathogenic T cells in coeliac disease. Lancet. 2003;362:30–37

PII: S0016-5085(09)00101-2

doi:10.1053/j.gastro.2009.01.038

Gastroenterology
Volume 136, Issue 3 , Pages 739-740, March 2009

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