Oat sensitivity

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Oat sensitivity represents a sensitivity to the proteins found in oats, Avena sativa. Sensitivity to oats as a result of allergy or to the seed storage proteins either inhaled or ingested. A more complex condition results to individuals who have gluten-sensitive enteropathy in which there is also a response to avenin, the glutinous protein in oats similar to the gluten within wheat.

Oat allergy

Template:Gluten sensitivity Studies on farmers with grain dust allergy and children with atopy dermatitis reveal that oat proteins can act as both respiratory and skin allergens.[1][2][3][4][5] Oat-dust sensitivity in farms found 53% showed reactivity to dust second only to barley (70%) and almost double that of wheat dust.[6] The 66 kDa protein in oats was visualized by 28 out of 33 sera (84%), however, there was evident non-specific binding to this region and thus it may also represent lectin-like binding.[7] However, IgA and IgG responses, like those seen to anti-gliadin antibodies in celiac disase or dermatitis herpetiformis, are not seen to avenins in atopic dermatitis patients.[8] Food allergies to oats can accompany atopy dermatitis.[9] Oat avenins share similarities with γ and ω-gliadins of wheat, based on these similarities they could potentiate both enteropathic response and anaphylactic responses. Oat allergy in gluten-sensitive enteropathy can explain an avenin sensitive individual who no histological abnormality, no T-cell reaction to avenin, bore the rarer DQ2.5trans phenotype and had anaphylactic reaction to avenin.[10]

Further information: [[:Wheat allergy]]

and Wheat dependent exercise-induced anaphylaxis

Avenin-sensitive enteropathy

Gluten-sensitive enteropathy and its common and more severe form, coeliac disease, results in the increased inflammation of the tissues of the small bowel eventually leading to villus atrophy. The disease progresses from increase lymphocyte counts to eventual flattening of the villi and crypt hyperplasia. Originally, oats were believed to cause coeliac disease, however this confusion was largely due to significant contamination of oats with wheat, barley or rye. A recent review of controlled oat tolerance studies indicated only one documented avenin-sensitive enteropathy(ASE) in 165, placing the risk of ASE at 0.6% of coeliac disease population.[11]

Further information: [[:The oat controversy in gluten sensitivity]]

Immunological evidence

Anti-avenin antibodies

In 1992, 6 protein were extracted from oats that reacted with a single coeliac sera. The proteins, prolamins, were called CIP 1 (gamma avenin), CIP 2 , and CIP3. The had the following amino-acid sequences: 

Antibody recognition sites on three avenins
CIP1 (γ-avenin)               P S E Q Y Q P Y P E Q Q Q P F 
CIP2 (γ-avenin) T T T V Q Y D P S E Q Y Q P Y P E Q Q Q P F V Q Q Q P P F 
CIP3 (α-avenin) T T T V Q Y N P S E Q Y Q P Y

within the same paper 3 other protiens were identified, one was an α-amylase inhibitor, identified by protein homology. A follow-up study showed that most celiacs have anti-avenin antibodies(AVA), with a specificity and sensitivity comparable to anti-gliadin antibodies.[12] A subsequent study found that these AVA did not result from cross-reaction with wheat. [13] However recently it has been found that AVA drop as soon as Triticeae glutens are removed from the diet.[14] Anti-avenin antibodies decline in treated celiacs on an oat diet in 136 individuals this suggests that oats can be involved in celiac disease when wheat is present, but is not involved when wheat is removed from the diet. The study however did find an increase number of patients with higher intra-epithelial lymphocytes (IEL) in the oat eating cohort.

Cellular immunity

In gluten-sensitive enteropathy, prolamins mediate between T-cells and antigen presenting cells, whereas anti-transglutaminase antibodies confer autoimmunity via covelant attachment to gliadin. In 16 examined coeliacs, none produced a significant Th1 response [15] Th1 responses are needed to stimulate the T-helper cells that mediated disease. This could indicate that avenins could not involve in coeliac disease or that the sample size was too small to detect the occasional responder.

Evidence that there are exceptional cases came in a 2004 study on oats.[10] The patients drafted for this study were those who had symptoms of celiac disease when on an 'pure-oat' challenge, therefore they do not represent the random population of celiacs. This study found that 4 patients had symptoms after oat ingestion, 3 had elevated Marsh scores for histology, and avenin responsive T-cells, indicating avenin-sensitive enteropathy(ASE). All three patients were DQ2.5/DQ2 (HLA DR3-DQ2/DR7-DQ2) phenotype. Patients with DQ2.5/DQ2.2 tend to be the most prone toward GSE, have the highest risk for GS-EATL, and shows signs of more severe disease at diagnosis. While DQ2.5/DQ2 phenotype represents only 25% of celiac patients, it accounts for all of the ASE celiacs, and 60-70% of patients with GS-EATL. Synthetic avenin peptides were synthesized either in native or deamidated form, the deamidated peptides showed higher response. 

DQ2.5/T-cell receptor recognition from 2 Oat-sensitive coeliacs
TCR-Site1                             Y Q P Y P E Q E~E~P F V
TCR-Site2                           Q Y Q P Y P E Q Q Q P F V Q Q Q Q
Antibody recognition site(see above)
CIP2 (γ-avenin) T T T V Q Y D P S E Q Y Q P Y P E Q Q Q P F V Q Q Q P P F

The overlap of the antibody and T-cell sites, given trypsin digestion of avenin, suggest this region is dominant in immunity. The TCR-site1 was synthetically made as deamidated ("~E~") and native peptide requires transglutaminase to reach full activation. Two studies to date have looked at the ability for different oat-strains to promote various immunochemical aspects of celiac disease. While preliminary these studies indicate different strains may have different risk for avenin-sensitivity[16][17]


Oats and coeliac disease

Recent studies indicate both children and adult coeliacs are largely tolerant of oats.[18][19][20][21] Recent studies have followed both children and adults for 1, 2 and 5 years on the 'uncontaminated'-oat[22] containing gluten-free diet.[23][24][25][26][27] These studies failed to show significant changes in intestinal morphology indication a relapse of celiac disease. Anti-gliadin and reticulin antibodies as well as numbers of intraepithelial lymphocytes (IELs) did not differ significantly between oat-eating celiacs and non-oat eating controls in remission. [28] Invrito tests that are sensitive to wheat gluten found that tryptic peptides of avenin could not induce EMA production in supernatant fluid from cultured duodenal mucosa specimen from celiac patients. [29] Algorithms that successfully predict T cell stimulatory peptides in gluten identified many similar peptides in hordeins and secalins but not in oat avenins.[30] The Canadian Celiac Association suggests that adults can consume up to 70 g of oats and children up to 25 g per day,[31] however, two studies indicated that adults could consume 93 grams (3.3 ounces) of oats per day. There is no evidence that oats can trigger GSE, only that in a small number of celiacs disease can be sustained or reinitiated by oats once triggered by wheat. A recent paper examining the IEL of celiac patients in remission showed a significantly higher number of IEL in oat eating celiacs, in addition antibodies to Avenin remain low as long as the diet is gluten -free but higher anti-avenin antibodies can increase with a diet containing wheat.

Further information: [[:The oat controversy in gluten sensitivity]]

Some coeliacs respond adversely to oats. Estimates range from 0.5 to 20% of the GSE population. With coeliac disease non-compliance to achieve normal intestinal morphology is a risk factor for refractory disease and cancer.

(See GSE associated cancers).

Further information: [[:Cancers and Refractory disease associated with gluten-sensitivity]]

References

  1. ↑ Boussault P, Léauté-Labrèze C, Saubusse E; et al. (2007). "Oat sensitization in children with atopic dermatitis: prevalence, risks and associated factors". Allergy. 62 (11): 1251–6. doi:10.1111/j.1398-9995.2007.01527.x. PMID 17919139. Unknown parameter |month= ignored (help)
  2. ↑ Codreanu F, Morisset M, Cordebar V, Kanny G, Moneret-Vautrin DA (2006). "Risk of allergy to food proteins in topical medicinal agents and cosmetics". Eur Ann Allergy Clin Immunol. 38 (4): 126–30. PMID 16805419. Unknown parameter |month= ignored (help)
  3. ↑ De Paz Arranz S, Pérez Montero A, Remón LZ, Molero MI (2002). "Allergic contact urticaria to oatmeal". Allergy. 57 (12): 1215. PMID 12464060. Unknown parameter |month= ignored (help)
  4. ↑ Pazzaglia M, Jorizzo M, Parente G, Tosti A (2000). "Allergic contact dermatitis due to avena extract". Contact Derm. 42 (6): 364. PMID 10871113. Unknown parameter |month= ignored (help)
  5. ↑ Baldo BA, Krilis S, Wrigley CW (1980). "Hypersensitivity to inhaled flour allergens. Comparison between cereals". Allergy. 35 (1): 45–56. PMID 6154431. Unknown parameter |month= ignored (help)
  6. ↑ Manfreda J, Holford-Strevens V, Cheang M, Warren CP (1986). "Acute symptoms following exposure to grain dust in farming". Environ. Health Perspect. 66: 73–80. PMC 1474397. PMID 3709486. Unknown parameter |month= ignored (help)
  7. ↑ Varjonen E, Savolainen J, Mattila L, Kalimo K (1994). "IgE-binding components of wheat, rye, barley and oats recognized by immunoblotting analysis with sera from adult atopic dermatitis patients". Clin. Exp. Allergy. 24 (5): 481–9. PMID 8087661. Unknown parameter |month= ignored (help)
  8. ↑ Varjonen E, Kalimo K, Savolainen J, Vainio E (1996). "IgA and IgG binding components of wheat, rye, barley and oats recognized by immunoblotting analysis with sera from adult atopic dermatitis patients". Int. Arch. Allergy Immunol. 111 (1): 55–63. PMID 8753845. Unknown parameter |month= ignored (help)
  9. ↑ Estrada-Reyes E, Hernnández-Román MP, Gamboa-Marrufo JD, Valencia-Herrera A, Nava-Ocampo AA (2008). "Hypereosinophilia, hyper-IgE syndrome, and atopic dermatitis in a toddler with food hypersensitivity". J Investig Allergol Clin Immunol. 18 (2): 131–5. PMID 18447144.
  10. ↑ 10.0 10.1 Arentz-Hansen H, Fleckenstein B, Molberg Ø; et al. (2004). "The molecular basis for oat intolerance in patients with celiac disease". PLoS Med. 1 (1): e1. doi:10.1371/journal.pmed.0010001. PMC 523824. PMID 15526039. Unknown parameter |month= ignored (help)
  11. ↑ Garsed K, Scott BB (2007). "Can oats be taken in a gluten-free diet? A systematic review". Scand. J. Gastroenterol. 42 (2): 171–8. doi:10.1080/00365520600863944. PMID 17327936. Unknown parameter |month= ignored (help)
  12. ↑ Ribes-Koninckx C, Alfonso P, Ortigosa L; et al. (2000). "A beta-turn rich oats peptide as an antigen in an ELISA method for the screening of coeliac disease in a paediatric population". Eur. J. Clin. Invest. 30 (8): 702–8. PMID 10964162. Unknown parameter |month= ignored (help)
  13. ↑ Hollén E, Högberg L, Stenhammar L, Fälth-Magnusson K, Magnusson KE (2003). "Antibodies to oat prolamines (avenins) in children with coeliac disease". Scand. J. Gastroenterol. 38 (7): 742–6. PMID 12889560. Unknown parameter |month= ignored (help)
  14. ↑ Guttormsen V, Løvik A, Bye A, Bratlie J, Mørkrid L, Lundin KE (2008). "No induction of anti-avenin IgA by oats in adult, diet-treated coeliac disease". Scand. J. Gastroenterol. 43 (2): 161–5. doi:10.1080/00365520701832822. PMID 18224563.
  15. ↑ Kilmartin C, Lynch S, Abuzakouk M, Wieser H, Feighery C (2003). "Avenin fails to induce a Th1 response in coeliac tissue following in vitro culture". Gut. 52 (1): 47–52. PMC 1773501. PMID 12477758. Unknown parameter |month= ignored (help)
  16. ↑ Silano M, Di Benedetto R, Maialetti F; et al. (2007). "Avenins from different cultivars of oats elicit response by coeliac peripheral lymphocytes". Scand. J. Gastroenterol. 42 (11): 1302–5. doi:10.1080/00365520701420750. PMID 17852883. Unknown parameter |month= ignored (help)
  17. ↑ Silano M, Dessì M, De Vincenzi M, Cornell H (2007). "In vitro tests indicate that certain varieties of oats may be harmful to patients with coeliac disease". J. Gastroenterol. Hepatol. 22 (4): 528–31. doi:10.1111/j.1440-1746.2006.04512.x. PMID 17376046. Unknown parameter |month= ignored (help)
  18. ↑ Dissanayake AS, Truelove SC, Whitehead R (1974). "Lack of harmful effect of oats on small-intestinal mucosa in coeliac disease". Br Med J. 4 (5938): 189–91. PMC 1612349. PMID 4417208. Unknown parameter |month= ignored (help)
  19. ↑ Janatuinen EK, Pikkarainen PH, Kemppainen TA; et al. (1995). "A comparison of diets with and without oats in adults with celiac disease". N. Engl. J. Med. 333 (16): 1033–7. PMID 7675045. Unknown parameter |month= ignored (help)
  20. ↑ Srinivasan U, Leonard N, Jones E; et al. (1996). "Absence of oats toxicity in adult coeliac disease". BMJ. 313 (7068): 1300–1. PMC 2352731. PMID 8942690. Unknown parameter |month= ignored (help)
  21. ↑ Hoffenberg EJ, Haas J, Drescher A; et al. (2000). "A trial of oats in children with newly diagnosed celiac disease". J. Pediatr. 137 (3): 361–6. doi:10.1067/mpd.2000.109003. PMID 10969261. Unknown parameter |month= ignored (help)
  22. ↑ "patients used oat products from major Finnish mills. These products have been found to be free of contamination" Authors’ reply - Oats and celiac disease
  23. ↑ Janatuinen EK, Kemppainen TA, Julkunen RJ; et al. (2002). "No harm from five year ingestion of oats in coeliac disease". Gut. 50 (3): 332–5. PMC 1773136. PMID 11839710. Unknown parameter |month= ignored (help)
  24. ↑ Dor R, Shanahan DJ (2002). "Oats and coeliac disease". Gut. 51 (5): 757, author reply 757–8. PMC 1773434. PMID 12377824. Unknown parameter |month= ignored (help)
  25. ↑ Størsrud S, Olsson M, Arvidsson Lenner R, Nilsson LA, Nilsson O, Kilander A (2003). "Adult coeliac patients do tolerate large amounts of oats". Eur J Clin Nutr. 57 (1): 163–9. doi:10.1038/sj.ejcn.1601525. PMID 12548312. Unknown parameter |month= ignored (help)
  26. ↑ Högberg L, Laurin P, Fälth-Magnusson K; et al. (2004). "Oats to children with newly diagnosed coeliac disease: a randomised double blind study". Gut. 53 (5): 649–54. PMC 1774046. PMID 15082581. Unknown parameter |month= ignored (help)
  27. ↑ Holm K, Mäki M, Vuolteenaho N; et al. (2006). "Oats in the treatment of childhood coeliac disease: a 2-year controlled trial and a long-term clinical follow-up study". Aliment. Pharmacol. Ther. 23 (10): 1463–72. doi:10.1111/j.1365-2036.2006.02908.x. PMID 16669961. Unknown parameter |month= ignored (help)
  28. ↑ Janatuinen EK, Kemppainen TA, Pikkarainen PH; et al. (2000). "Lack of cellular and humoral immunological responses to oats in adults with coeliac disease". Gut. 46 (3): 327–31. PMC 1727854. PMID 10673292. Unknown parameter |month= ignored (help)
  29. ↑ Picarelli A, Di Tola M, Sabbatella L; et al. (2001). "Immunologic evidence of no harmful effect of oats in celiac disease". Am. J. Clin. Nutr. 74 (1): 137–40. PMID 11451729. Unknown parameter |month= ignored (help)
  30. ↑ Vader LW, de Ru A, van der Wal Y; et al. (2002). "Specificity of tissue transglutaminase explains cereal toxicity in celiac disease". J. Exp. Med. 195 (5): 643–9. PMC 2193762. PMID 11877487. Unknown parameter |month= ignored (help)
  31. ↑ Rashid M, Butzner D, Burrows V; et al. (2007). "Consumption of pure oats by individuals with celiac disease: a position statement by the Canadian Celiac Association". Can. J. Gastroenterol. 21 (10): 649–51. PMID 17948135. Unknown parameter |month= ignored (help)

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