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Wiener Medizinische Wochenschrift

, Volume 162, Issue 23–24, pp 513–518 | Cite as

Mechanisms and risk factors for type 1 food allergies: the role of gastric digestion

  • Susanne C. Diesner
  • Isabella Pali-Schöll
  • Erika Jensen-Jarolim
  • Eva UntersmayrEmail author
themenschwerpunkt

Summary

True food allergens are considered as digestion stable proteins, which are absorbed through the gastrointestinal epithelium in an intact form leading to sensitization and causing systemic symptoms. According to classifications, allergens, which are digestion-labile, cause local symptoms by their cross-reactivity towards inhalative allergens. Our recent studies revealed that digestion labile allergens can also have sensitizing capacity if gastric digestion is hindered. The increase of gastric pH via acid-suppression by proton pump inhibitors, sucralfate or antacids, interferes with protein digestion, and leads to sensitization and allergic reaction in mouse models as well as in human patients. Furthermore, the inhibition of digestion increases the risk for anaphylactic responses in sensitized individuals.

Even though also other factors, such as sphingolipid metabolites, are associated with the development of food allergies, it is without any doubt that the stomach has an important gate keeping function against food allergies.

Keywords

Food allergy Gastric digestion Antacids Anti-ulcus drugs 

Mechanismen und Risikofaktoren für Typ 1 Nahrungsmittelallergien: Die Rolle der gastrischen Verdauung

Zusammenfassung

Die sogenannten wahren Nahrungsmittelallergene sind verdauungsstabile Proteine, welche über das gastrointestinale Epithel in intakter Form aufgenommen werden und auf diesem Weg sensibilisieren und systemische Symptome auslösen können. Verdauungslabile Allergene andererseits führen laut Klassifikation durch ihre Kreuzreaktivität mit inhalativen Allergenen zu lokalen Symptomen. Unsere rezenten Studien zeigten jedoch, dass auch verdauungslabile Allergene ein hohes Sensibilisierungs-Potential haben, wenn die Magenverdauung gehemmt wird. Eine Erhöhung des gastrischen pH-Wertes aufgrund von Magensäure-Suppression durch Protonenpumpen-Hemmer, Sucralfat oder Antazida, hemmen den Verdau von Proteinen und führen so zur Sensibilisierung und allergischen Reaktionen sowohl im Tiermodell als auch bei Patienten. Weiters erhöht eine Inhibierung der Magenverdauung bei bereits allergischen Patienten das Risiko für eine anaphylaktische Reaktion.

Obwohl auch andere Faktoren, wie beispielsweise Sphingolipid-Metaboliten, eine Rolle bei der Entstehung von Nahrungsmittelallergien spielen, hat der Magen ohne Zweifel eine wichtige Barrierefunktion gegen Nahrungsmittelallergiene.

Schlüsselwörter

Nahrungsmittelallergie Gastrische Verdauung Antazida Anti-Ulkus Therapeutika 

Notes

Danksagung

Unterstützt von den Projekten des Fonds zur Förderung der Wissenschaftlichen Forschung (FWF) P21577 P21884 sowie SFB F 4606-B19.^ und P21884.

Literatur

  1. 1.
    Bannon GA. What makes a food protein an allergen? Curr Allergy Asthma Rep. 2004;4(1):43–6.PubMedCrossRefGoogle Scholar
  2. 2.
    Nowak-Wegrzyn A. Food allergy to proteins. Nestle Nutr Workshop Ser Pediatr Program. 2007;59:17–31 (discussion 31–6).PubMedGoogle Scholar
  3. 3.
    Vieths S, Scheurer S, Ballmer-Weber B. Current understanding of cross-reactivity of food allergens and pollen. Ann N Y Acad Sci. 2002;964:47–68.PubMedCrossRefGoogle Scholar
  4. 4.
    Aalberse RC. Structural biology of allergens. J Allergy Clin Immunol. 2000;106:228–38.PubMedCrossRefGoogle Scholar
  5. 5.
    Webber CM, England RW. Oral allergy syndrome: a clinical, diagnostic, and therapeutic challenge. Ann Allergy Asthma Immunol. 2010;104(2):101–8 (quiz 109–10, 117).PubMedCrossRefGoogle Scholar
  6. 6.
    Directive 2003//EC of the European Parliament and of the Council of amending Directive 2000/13/EC as regards indication of the ingredients present in foodstuffs. http://www.europarl.eu.int/commonpositions/2003/pdf/c5-0080-03_en.pdf. Zugegriffen: 25. Sept. 2006.
  7. 7.
  8. 8.
    Food safety: regulating plant agricultural biotechnology in the United States. http://www.4uth.gov.ua/usa/english/tech/biotech/foodsafe.htm. Zugegriffen: 18. Okt. 2012.
  9. 9.
    Fu TJ, Abbott UR, Hatzos C. Digestibility of food allergens and nonallergenic proteins in simulated gastric fluid and simulated intestinal fluid-a comparative study. J Agric Food Chem. 2002;50(24):7154–60PubMedCrossRefGoogle Scholar
  10. 10.
    Untersmayr E, Schöll I, Swoboda I, et al. Antacid medication inhibits digestion of dietary proteins and causes food allergy: a fish allergy model in Balb/c mice. J Allergy Clin Immunol. 2003;112:616–23.PubMedCrossRefGoogle Scholar
  11. 11.
    Schöll I, Untersmayr E, Bakos N, et al. Antiulcer drugs promote oral sensitization and hypersensitivity to hazelnut allergens in BALB/c mice and humans. Am J Clin Nutr. 2005;81:154–60.PubMedGoogle Scholar
  12. 12.
    Untersmayr E, Jensen-Jarolim E. The effect of gastric digestion on food allergy. Curr Opin Allergy Clin Immunol. 2006;6:214–9.PubMedCrossRefGoogle Scholar
  13. 13.
    Untersmayr E, Poulsen LK, Platzer MH, et al. The effects of gastric digestion on codfish allergenicity. J Allergy Clin Immunol. 2005;115:377–82.PubMedCrossRefGoogle Scholar
  14. 14.
    Untersmayr E, Bakos N, Schöll I, et al. Anti-ulcer drugs promote IgE formation toward dietary antigens in adult patients. FASEB J. 2005;19:656–8.PubMedGoogle Scholar
  15. 15.
    Untersmayr E, Jensen-Jarolim E. Anti-azide Therapie und verdauungslabile Allergene. Allergologie. 2005;28(4):134–42.Google Scholar
  16. 16.
    Diesner SC, Knittelfelder R, Krishnamurthy D, et al. Dose-dependent food allergy induction against ovalbumin under acid-suppression: a murine food allergy model. Immunol Lett. 2008;121(1):45–51.PubMedCrossRefGoogle Scholar
  17. 17.
    Samloff IM. Peptic ulcer: the many proteinases of aggression. Gastroenterology. 1989;96:586–95.PubMedGoogle Scholar
  18. 18.
    Avery GB, Randolph JG, Weaver T. Gastric acidity in the first day of life. Pediatrics. 1966;37:1005–7.PubMedGoogle Scholar
  19. 19.
    Ebers DW, Gibbs GE, Smith DI. Gastric acidity on the first day of life. Pediatrics. 1956;18:800–2.PubMedGoogle Scholar
  20. 20.
    Agunod M, Yamaguchi N, Lopez R, et al. Correlative study of hydrochloric acid, pepsin, and intrinsic factor secretion in newborns and infants. Am J Dig Dis. 1969;14:400–14.PubMedCrossRefGoogle Scholar
  21. 21.
    Deren JS. Development of structure and function in the fetal and newborn stomach. Am J Clin Nutr. 1971;24:144–59.PubMedGoogle Scholar
  22. 22.
    Segawa K, Nakazawa S, Tsukamoto Y, et al. Chronic alcohol abuse leads to gastric atrophy and decreased gastric secretory capacity: a histological and physiological study. Am J Gastroenterol. 1988;83(4):373–9.PubMedGoogle Scholar
  23. 23.
    Brunner R, Wallmann J, Szalai K, et al. Aluminium per se and in the anti-acid drug sucralfate promotes sensitization via the oral route. Allergy. 2009;64(6):890–7.PubMedCrossRefGoogle Scholar
  24. 24.
    Brunner R, Wallmann J, Szalai K, et al. The impact of aluminium in acid-suppressing drugs on the immune response of BALB/c mice. Clin Exp Allergy. 2007;37(10):1566–73.PubMedCrossRefGoogle Scholar
  25. 25.
    Pali-Schöll I, Herzog R, Wallmann J, et al. Antacids and dietary supplements with an influence on the gastric pH increase the risk for food sensitization. Clin Exp Allergy. 2010;40(7):1091–8.PubMedCrossRefGoogle Scholar
  26. 26.
    Diesner SC, Olivera A, Dillahunt S, et al. Sphingosine-kinase 1 and 2 contribute to oral sensitization and effector phase in a mouse model of food allergy. Immunol Lett. 2012;141(2):210–9.PubMedCrossRefGoogle Scholar
  27. 27.
    Untersmayr E., Ellinger A., Beil WJ., et al. Eosinophils accumulate in the gastric mucosa of food allergic mice. Int Arch Allergy Immunol. 2004;135(1)1–2.Google Scholar
  28. 28.
    Pali-Schöll I, Yildirim AO, Ackermann U, et al. Anti-acids lead to immunological and morphological changes in the intestine of BALB/c mice similar to human food allergy. Exp Toxicol Pathol. 2008;60(4–5):337–45.CrossRefGoogle Scholar
  29. 29.
    Untersmayr E, Diesner SC, Bramswig KH, et al. Characterization of intrinsic and extrinsic risk factors for celery allergy in immunosenescence. Mech Ageing Dev. 2008;129(3):120–8.PubMedCrossRefGoogle Scholar
  30. 30.
    Miller R. The aging immune system: primer and prospectus. Science. 1996;273:70–4.PubMedCrossRefGoogle Scholar
  31. 31.
    Branum AM, Lukacs SL. Food allergy among children in the United States. Pediatrics. 2009;124(6):1549–55.PubMedCrossRefGoogle Scholar
  32. 32.
    Wöhrl S, Stingl G. Underestimation of allergies in elderly patients. Lancet North Am Ed. 2004;363:249.CrossRefGoogle Scholar
  33. 33.
    Richter JE. Gastroesophageal reflux disease during pregnancy. Gastroenterol Clin North Am. 2003;32(1):235–61.PubMedCrossRefGoogle Scholar
  34. 34.
    Schöll I, Ackermann U, Ozdemir C, et al. Anti-ulcer treatment during pregnancy induces food allergy in mouse mothers and a Th2-bias in their offspring. FASEB J. 2007;21(4):1264–70.PubMedCrossRefGoogle Scholar
  35. 35.
    Bakos N, Schöll I, Szalai K, et al. Risk assessment in elderly for sensitization to food and respiratory allergens. Immunol Lett. 2006;107:15–21.PubMedCrossRefGoogle Scholar
  36. 36.
    Hsu RY, Lin MS, Chou MH, et al. Medication use characteristics in an ambulatory elderly population in Taiwan. Ann Pharmacother. 1997;31(3):308–14.PubMedGoogle Scholar
  37. 37.
    Pali-Schöll I, Jensen-Jarolim E. Anti-acid medication as a risk factor for food allergy. Allergy. 2011;66(4):469–77.PubMedCrossRefGoogle Scholar
  38. 38.
    Untersmayr E, Jensen-Jarolim E. The role of protein digestibility and antacids on food allergy outcomes. J Allergy Clin Immunol. 2008;121(6):1301–8 (quiz 1309–10).PubMedCrossRefGoogle Scholar
  39. 39.
    Untersmayr E, Vestergaard H, Malling HJ, et al. Incomplete digestion of codfish represents a risk factor for anaphylaxis in patients with allergy. J Allergy Clin Immunol. 2007;119(3):711–7.PubMedCrossRefGoogle Scholar
  40. 40.
    Hannun YA, Luberto C, Argraves KM. Enzymes of sphingolipid metabolism: from modular to integrative signaling. Biochemistry. 2001;40(16):4893–903.PubMedCrossRefGoogle Scholar
  41. 41.
    Spiegel S, Milstien S. Sphingosine-1-phosphate: an enigmatic signalling lipid. Nat Rev Mol Cell Biol. 2003;4(5):397–407.PubMedCrossRefGoogle Scholar
  42. 42.
    Olivera A, Eisner C, Kitamura Y, et al. Sphingosine kinase 1 and sphingosine-1-phosphate receptor 2 are vital to recovery from anaphylactic shock in mice. J Clin Invest. 2010;120(5):1429–40.PubMedCrossRefGoogle Scholar
  43. 43.
    Hait NC, Oskeritzian CA, Paugh SW, et al. Sphingosine kinases, sphingosine 1-phosphate, apoptosis and diseases. Biochim Biophys Acta. 2006;1758(12):2016–26.PubMedCrossRefGoogle Scholar
  44. 44.
    Yunoki K, Ogawa T, Ono J, et al. Analysis of sphingolipid classes and their contents in meals. Biosci Biotechnol Biochem. 2008;72(1):222–5.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Wien 2012

Authors and Affiliations

  • Susanne C. Diesner
    • 1
    • 2
  • Isabella Pali-Schöll
    • 1
    • 3
  • Erika Jensen-Jarolim
    • 1
    • 3
  • Eva Untersmayr
    • 1
    Email author
  1. 1.Institut für Pathophysiologie und Allergieforschung, Zentrum für Pathophysiologie, Infektiologie und ImmunologieMedizinische Universität WienWienÖsterreich
  2. 2.Universitätsklinik für Kinder- und Jugendheilkunde Medizinische Universität WienWienÖsterreich
  3. 3.Messerli Forschungsinstitut der VeterinärmedizinischenUniversität Wien, Medizinische Universität Wien, und Universität WienWienÖsterreich

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