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Are Non-Celiac Autoimmune Diseases Responsive to Gluten-Free Diet?

Aaron Lerner, Ajay Ramesh, Torsten Matthias
International Journal of Celiac Disease. 2017, 5(4), 164-167. DOI: 10.12691/ijcd-5-4-6
Published online: November 24, 2017

Abstract

Genetic risk factors for autoimmune diseases are constantly discovered, however, environmental factors are laggingbehind and the precipitating events leading to development of autoimmune diseases remain enigmatic. Gluten is a well-established inducing nutrient in celiac disease and gluten withdrawal is the only current effective therapy. More and more studies have shown that non-celiac autoimmune diseases can partially respond to gluten free diet. The present editorial reviews those conditions and suggest multiple potential mechanisms that might operate in clinical amelioration of non-celiac autoimmune diseases.

1. Introduction

It is well known that autoimmune diseases (ADs) have two major causative background: genetic and environmental 1, 2, 3. Due to the fact that ADs incidence is markedly increased in the Western countries in the last decades 4, 5, it is logical to assume that the surge is due to changing environment, much more than genetic modifications or adaptations. Taking into account that the worldwide wheat consumption and gluten intake are likewise increasing, in the last decades 6, it is tempting to speculate that a positive association exist between the two and the surge of ADs. There is no doubt that, at least for celiac disease (CD), the increase in prevalence is tightly relayed to the increased wheat consumption around the world 4, 7. Since CD is associated with multiple ADs, a question arises does gluten consumption contribute to the surge in the non-CD autoimmune conditions and if so, does gluten withdrawal might as well benefit the autoimmune affected populations.

In this regard, the case reported by the Iranian group on the positive effect of gluten-free diet (GFD) in refractory inflammatory bowel disease is very interesting 8 and brings up the topic of GFD in non-CD autoimmune condition. Rostami-Nejad et al. described a young male with refractory left-sided ulcerative colitis with normal bulbar and duodenal biopsies and CD associated serology. Upon GFD, his symptoms disappeared and the colonic pathology improved. It should be noted that other recent reports on Crohn’s disease patients reported that GFD might be beneficial in reducing gastrointestinal symptoms, disease activity index and drug responsiveness 9, 10, 11. The present editorial will review the non-CD ADs that under certain circumstances responded to GFD, and the potential mechanism relaying gluten withdrawal to the improvement of autoimmune diseases and their responsiveness.

2. GFD in none Classical Gluten Dependent Autoimmune Conditions

The subject of GFD in other peripheral, non-enteric ADs was reviewed in the past 12, 13 and most recently extensively described 14. Interestingly, in a most recent editorial on the subject of indications for GFD, those non-CD, systemic ADs were not mentioned 15.

3. Potential Mechanisms of Gluten Free Nutritional Therapy in Non-Enteric Autoimmune Diseases

The list of all diseases in Table 1 is associated with CD and GFD 39 and multiple autoantibodies that are circulating in the patient’s blood circulation 40. Suspicions about the benefit of GFD as a complementary treatment, either as a causal factor in the pathogenesis, or improvement of symptoms, was raised and reviewed lately 41, 42.The fact that GFD have protective effects on the cumulative prevalence of additional autoimmune diseases in CD patients 43, 44, opens a window of opportunities to explore the topic of gluten as a driver of autoimmunity and the place of GFD in ADs dietary therapy.

Not less interesting are the potential pathways by which gluten withdrawal might impact the initiation and the progression of autoimmunity. Following are some of those potential mechanisms.

a. Shared genes. CD shares HLA and various non-HLA genes with associated ADs 45, 46, 47, 48.

b. Increases intestinal permeability and leaky gut induction. Various processed food ingredients and additives were proved or suspected to breach tight junction functional integrity 6, 39.Gluten is one of them 6, 49, 50. WillGFD attenuate the leaky gut process?

c. Microbiome/dysbiome imbalance. The dysbiotic repertoire related to animal models of specific ADs was recently summarized 3, and multiple publications exist on the dysbiosis in CD and other human ADs 39, 51. Gluten affects microbiome composition and diversity as shown in animal models and on humans 14, 39. Can gluten drive systemic autoimmunity through its effects on the human microbiome?

d. Pro-inflammatory and potentially auto immunogenic effects. Gluten is immunogenic, cytotoxic, pro-inflammatory and activates several immune pathways (including IL-17). It increases apoptosis, suppresses cell viability and differentiation, induces oxidative stress and affects epigenetic behavior 14.

e. Increased amount, toxicity and immunogenicity. Contemporary gluten has evolved tremendously since its discovery in the Fertile Crescent around 15000 years ago 2. The wheat gluten content increased about 8 folds, its worldwide consumption expanded, its toxicity and immunogenicity rose and created a geoepidemiology. This dynamics paralleled the increased incidence of CD and other ADs 2, 4, 5, 52, 53

f. Intestinal post translational modification of protein (PTMP) represents a key regulator in autoimmunity, by transforming naïve/self or non-self-peptides to auto immunogenic ones. 3, 39, 54. Gluten is an ideal substrate for enzymatic PTMP, tissue and microbial transglutaminases being typical examples 3, 54, 55, 56.

g. Tissue and microbial transglutaminases are extensively distributed in the human body and intestinal lumen, respectively 39, 54, 57. Human transglutaminase plays a role in end organ affected ADs. Autoimmune thyroiditis, rheumatoid arthritis, IgA nephropathy, dermatitis herpetiformis and gluten ataxia are some of the examples 58, 59, 60, 61, 62, 63. On the other hand, gluten/gliadin peptides are internalized systemically and are secreted in the human urine 64, 65, or appear in the mice pancreas following oral administration 66. One wonders if in the absence of gluten, no immunogenic or neo-epitopes’ complexes will be available to drive autoimmunity.

h. HLA-DQ2/8-restricted gluten specific T cells have been observed to migrate from the intestinal lamina propria into peripheral blood upon gluten challenge, representing an additional mechanism for extraintestinal manifestations in CD, or potentially reaching peripheral organs in other ADs and thus, ameliorated on GFD 67.

4. Conclusions

We are far away from unraveling the mechanisms by which GFD can alleviate non-celiac ADs initiation or progression and there are more questions than answers on this very challenging topic.

References

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Published with license by Science and Education Publishing, Copyright © 2017 Aaron Lerner, Ajay Ramesh and Torsten Matthias

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Cite this article:

Normal Style
Aaron Lerner, Ajay Ramesh, Torsten Matthias. Are Non-Celiac Autoimmune Diseases Responsive to Gluten-Free Diet?. International Journal of Celiac Disease. Vol. 5, No. 4, 2017, pp 164-167. http://pubs.sciepub.com/ijcd/5/4/6
MLA Style
Lerner, Aaron, Ajay Ramesh, and Torsten Matthias. "Are Non-Celiac Autoimmune Diseases Responsive to Gluten-Free Diet?." International Journal of Celiac Disease 5.4 (2017): 164-167.
APA Style
Lerner, A. , Ramesh, A. , & Matthias, T. (2017). Are Non-Celiac Autoimmune Diseases Responsive to Gluten-Free Diet?. International Journal of Celiac Disease, 5(4), 164-167.
Chicago Style
Lerner, Aaron, Ajay Ramesh, and Torsten Matthias. "Are Non-Celiac Autoimmune Diseases Responsive to Gluten-Free Diet?." International Journal of Celiac Disease 5, no. 4 (2017): 164-167.
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[1]  Lerner A, Blank M, Shoenfeld Y. Celiac disease and autoimmunity.Isr J Med Sci 1996; 32: 33-36.
In article      PubMed
 
[2]  Lerner A. The last two millennias eco-catastrophes are the driving forces for the potential genetic advantage mechanisms in celiac disease. Med Hypotheses. 2011; 77: 773-6.
In article      View Article  PubMed
 
[3]  Lerner A, Aminov R, Matthias T. Dysbiosis may trigger autoimmune diseases via inappropriate posttranslational modification of host proteins. Front in Microbiol.2016; 7: 84.
In article      View Article  PubMed
 
[4]  Lerner A, Jermias P, Matthias T. The world incidence of celiac disease is increasing: a review. Internat. J. Of Recent Scient. Res. 2015; 7: 5491-5496.
In article      View Article
 
[5]  Lerner A, Jeremias P, Matthias T. The world incidence and prevalence of autoimmune diseases is increasing: A review. Internat J Celiac Disease. 2015; 3: 151-155.
In article      View Article
 
[6]  Lerner A, Matthias T. Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease. Autoimmun Rev. 2015; 14: 479-89.
In article      View Article  PubMed
 
[7]  Catassi C, Gatti S, Lionetti E. World perspective and celiac disease epidemiology. Dig Dis. 2015; 33: 141-6.
In article      View Article  PubMed
 
[8]  Rostami-Nejad M, Sadeghi A, Asadzadeh-Aghdaei H, Rismantab S, Reza Zali M. Gluten-free Diet for Refractory Inflammatory Bowel Disease; A Case Report. Internatiol J of Celiac Dis. 2017, 5: 168-170.
In article      View Article
 
[9]  Catassi C, Elli L, Bonaz B, Bouma G, Carroccio A, Castillejo G, et al. Diagnosis of Non-CeliacGluten Sensitivity (NCGS): The Salerno Experts' Criteria. Nutrients. 2015; 7: 4966-77.
In article      View Article  PubMed
 
[10]  Aziz I, Pearson K, Priest J, Sanders D. A Study Evaluating the Bidirectional Relationship Between Inflammatory Bowel Disease and Self-reported Non-celiac Gluten Sensitivity. Inflamm Bowel Dis 2015; 21: 847-53.
In article      View Article  PubMed
 
[11]  Hans H ,Christopher F, Robert S, Michael D, Millie D. Prevalence of a Gluten-free Diet and Improvement of Clinical Symptoms in Patients with Inflammatory Bowel Diseases. Inflamm Bowel Dis 2014; 20: 1194-7.
In article      View Article  PubMed
 
[12]  San Mauro Martín I, Garicano Vilar E, Collado Yurrutia L, Ciudad Cabañas MJ. [Is gluten the great etiopathogenic agent of disease in the XXI century?]. Nutricion Hospitalaria. 2014; 30: 1203-10.
In article      PubMed
 
[13]  El-Chammas K, Danner E. Gluten-free diet in nonceliac disease. Nutr in Clin Pract 2011; 26: 294-9.
In article      View Article  PubMed
 
[14]  Lerner A, Shoenfeld Y, Matthias T. Gluten; essential for wheat survival but detrimental to human health. Nutr Rev. In press. 2017.
In article      
 
[15]  Rostami K, Bold J, Parr A, Johnson MW. Gluten-Free Diet Indications, Safety, Quality, Labels, and Challenges. Nutrients. 2017 Aug 8; 9(8). pii: E846.
In article      View Article  PubMed
 
[16]  Hafström I, Ringertz B, Spångberg A, von Zweigbergk L, Brannemark S, Nylander I, Rönnelid J, Laasonen L, Klareskog L. A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: the effects on arthritis correlate with a reduction in antibodies to food antigens. Rheumatol (Oxford) 2001; 40: 1175-9.
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