Role of the Epidermal Barrier in the Formation of Food Allergies in Children with Genodermatosis
https://doi.org/10.15690/pf.v16i4.2053
Abstract
The article analyzes the most significant genodermatoses associated with a high risk of allergic reactions that may occur in the practice of a dermatologist and pediatrician, such as ichthyosis and ichthyosiform dermatoses, Netherton syndrome and other ichthyosiform erythroderma, peeling skin syndrome, SAM syndrome, as well as congenital bullous epidermolysis. The article also describes in detail the pathogenetic aspects of transcutaneous sensitization, the development of food allergies and the listed above genodermatoses, two illustrative clinical cases are given.
About the Authors
Nikolay N. Murashkin
National Medical Research Center for Children’s Health;
I.M. Sechenov First Moscow State Medical University (Sechenov University);
Central State Medical Academy of the Administrative Department of the President of the Russian Federation
Russian Federation
Moscow
Russian Federation
Moscow
Roman A. Ivanov
National Medical Research Center for Children’s Health
Russian Federation
Moscow
Russian Federation
Moscow
A. A. Savelova
National Medical Research Center for Children’s Health
Russian Federation
Moscow
Russian Federation
Moscow
D. V. Fedorov
National Medical Research Center for Children’s Health
Russian Federation
Moscow
Russian Federation
Moscow
L. A. Opryatin
National Medical Research Center for Children’s Health
Russian Federation
Moscow
Russian Federation
Moscow
Wasel Ahmad
Kabardino-Balkarian State University named after H.M. Berbekov
Russian Federation
Kabardino-Balkarian Republic
Russian Federation
Kabardino-Balkarian Republic
References
1. Sicherer SH, Allen K, Lack G, et al. Critical issues in food allergy: A National Academies Consensus Report. Pediatrics. 2017;140(2). pii: e20170194. doi: 10.1542/peds.2017-0194.
2. Lodge CJ, Allen KJ, Lowe AJ, et al. Overview of evidence in prevention and aetiology of food allergy: a review of systematic reviews. Int J Environ Res Public Health. 2013;10(11):5781–5806. doi: 10.3390/ijerph10115781.
3. Sicherer SH, Sampson HA. Food allergy: epidemiology, pathogenesis, diagnosis, and treatment. J Allergy Clin Immunol. 2014;133(2):291–307; quiz 308. doi: 10.1016/j.jaci.2013.11.020.
4. Jones SM, Burks AW. Food Allergy. N Engl J Med. 2017;377(12):1168–1176. doi: 10.1056/NEJMcp1611971.
5. Sicherer SH. Epidemiology of food allergy. J Allergy Clin Immunol. 2011;127(3):594–602. doi: 10.1016/j.jaci.2010.11.044.
6. Soller L, Ben-Shoshan M, Harrington DW, et al. Overall prevalence of self-reported food allergy in Canada. J Allergy Clin Immunol. 2012;130(4):986–988. doi: 10.1016/j.jaci.2012.06.029.
7. Nwaru BI, Hickstein L, Panesar SS, et al. The epidemiology of food allergy in Europe: a systematic review and meta-analysis. Allergy. 2014;69(1):62–75. doi: 10.1111/all.12305.
8. Loh W, Tang ML. The epidemiology of food allergy in the global context. Int J Environ Res Public Health. 2018;15(9). pii: E2043. doi: 10.3390/ijerph15092043.
9. McGowan EC, Keet CA. Prevalence of self-reported food allergy in the National Health and Nutrition Examination Survey (NHANES) 2007–2010. J Allergy Clin Immunol. 2013;132(5):1216–1219.e5. doi: 10.1016/j.jaci.2013.07.018.
10. Gupta RS, Warren CM, Smith BM, et al. The public health impact of parent-reported childhood food allergies in the United States. Pediatrics. 2018;142(6). pii: e20181235. doi: 10.1542/peds.2018–1235.
11. Loke P, Koplin J, Beck C, et al. Statewide prevalence of school children at risk of anaphylaxis and rate of adrenaline autoinjector activation in Victorian government schools, Australia. J Allergy Clin Immunol. 2016;138(2):529–535. doi: 10.1016/j.jaci.2016.02.014.
12. Hu Y, Chen J, Li H. Comparison of food allergy prevalence among Chinese infants in Chongqing, 2009 versus 1999. Pediatr Int. 2010;52(5):820–824. doi: 10.1111/j.1442-200X.2010.03166.x.
13. Yu W, Freeland DM, Nadeau KC. Food allergy: immune mechanisms, diagnosis and immunotherapy. Nat Rev Immunol. 2016;16(12):751–765. doi: 10.1038/nri.2016.111.
14. Mansoor DK, Sharma HP. Clinical presentations of food allergy. Pediatr Clin North Am. 2011;58(2):315–326, ix. doi: 10.1016/j.pcl.2011.02.008.
15. Bock SA, Muñoz-Furlong A, Sampson HA. Further fatalities caused by anaphylactic reactions to food, 2001–2006. J Allergy Clin Immunol. 2007;119(4):1016–1018. doi: 10.1016/j.jaci.2006.12.622.
16. Colver AF, Nevantaus H, Macdougall CF, Cant AJ. Severe foodallergic reactions in children across the UK and Ireland, 1998– 2000. Acta Paediatr. 2007;94(6):689–695. doi: 10.1111/j.16512227.2005.tb01966.x.
17. Berin MC, Shreffler WG. Mechanisms underlying induction of tolerance to foods. Immunol Allergy Clin North Am. 2016;36(1):87– 102. doi: 10.1016/j.iac.2015.08.002.
18. Worbs T, Bode U, Yan S, et al. Oral tolerance originates in the intestinal immune system and relies on antigen carriage by dendritic cells. J Exp Med. 2006;203(3):519–527. doi: 10.1084/jem.20052016.
19. Sampson HA, O’Mahony L, Burks AW, et al. Mechanisms of food allergy. J Allergy Clin Immunol. 2018;141(1):11–19. doi: 10.1016/j. jaci.2017.11.005.
20. Brown SJ, Asai Y, Cordell HJ, et al. Loss-of-function variants in the filaggrin gene are a significant risk factor for peanut allergy. J Allergy Clin Immunol. 2011;127(3):661–667. doi: 10.1016/j.jaci.2011.01.031.
21. Pishchevaya allergiya. Klinicheskie rekomendatsii [Internet]. Moscow: Soyuz pediatrov Rossii; 2018. (In Russ). Available from: http://www.pediatr-russia.ru/sites/default/files/file/kr_pa2018.pdf. Access date: 12.04.2019.
22. Posthumus J, James HR, Lane CJ, et al. Initial description of pork-cat syndrome in the United States. J Allergy Clin Immunol. 2013;131(3):923–925. doi: 10.1016/j.jaci.2012.12.665.
23. Brough HA, Liu AH, Sicherer S, et al. Atopic dermatitis increases the effect of exposure to peanut antigen in dust on peanut sensitization and likely peanut allergy. J Allergy Clin Immunol. 2015;135(1):164–170. doi: 10.1016/j.jaci.2014.10.007.
24. Amagai, Masayuki. The three musketeers of the epidermal barrier and atopic diseases. Cornea, 2014, November. 2014;33:S9. doi: 10.1097/ICO.0000000000000231.
25. Beck LA, Leung DY. Allergen sensitization through the skin induces systemic allergic responses. J Allergy Clin Immunol. 2000;106(5 Suppl):S258–263.
26. Bertelsen RJ, Faeste CK, Granum B, et al. Food allergens in mattress dust in Norwegian homes — a potentially important source of allergen exposure. Clin Exp Allergy. 2014;44(1):142–149. doi: 10.1111/cea.12231.
27. Izadi N, Luu M, Ong PY, Tam JS. The role of skin barrier in the pathogenesis of food allergy. Children (Basel). 2015;2(3):382–402. doi: 10.3390/children2030382.
28. Kubo A, Nagao K, Amagai M. Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases. J Clin Invest. 2012;122(2):440–447. doi: 10.1172/JCI57416.
29. Berin MC, Shreffler WG. T(h)2 adjuvants: implications for food allergy. J Allergy Clin Immunol. 2008;121(6):1311–1320; quiz 1321–1322. doi: 10.1016/j.jaci.2008.04.023.
30. Valenta R, Hochwallner H, Linhart B, Pahr S. Food allergies: the basics. Gastroenterology. 2015;148(6):1120–1131.e4. doi: 10.1053/j.gastro.2015.02.006.
31. Lexmond WS, Goettel JA, Sallis BF, et al. Spontaneous food allergy in Was-/mice occurs independent of FcεRI-mediated mast cell activation. Allergy. 2017;72(12):1916–1924. doi: 10.1111/all.13219.
32. Clark RA, Chong B, Mirchandani N, Mirchandani N. The vast majority of CLA+ T cells are resident in normal skin. J Immunol. 2006;176(7):4431–4439. doi: 10.4049/jimmunol.176.7.4431.
33. Lipscomb MF, Masten BJ. Dendritic cells: immune regulators in health and disease. Physiol Rev. 2002;82(1):97–130. doi: 10.1152/physrev.00023.2001.
34. Craiglow BG. Ichthyosis in the newborn. Semin Perinatol. 2013;37(1):26–31. doi: 10.1053/j.semperi.2012.11.001.
35. Oji V, Tadini G, Akiyama M, et al. Revised nomenclature and classification of inherited ichthyoses: results of the First Ichthyosis Consensus Conference in Sorèze 2009. J Am Acad Dermatol. 2010;63(4):607–641. doi: 10.1016/j.jaad.2009.11.020.
36. Wickett RR, Visscher MO. Structure and function of the epidermal barrier. Am J Infect Control. 2006;34(10, Suppl):S98–S110. doi: 10.1016/j.ajic.2006.05.295.
37. Egawa G, Kabashima K. Barrier dysfunction in the skin allergy. Allergol Int. 2018;67(1):3–11. doi: 10.1016/j.alit.2017.10.002.
38. Akiyama M. FLG mutations in ichthyosis vulgaris and atopic eczema: spectrum of mutations and population genetics. Br J Dermatol. 2010;162(3):472–477. doi: 10.1111/j.13652133.2009.09582.x.
39. Takeichi T, Okuno Y, Saito C, et al. Congenital ichthyosis and recurrent eczema associated with a novel ALOXE3 mutation. Acta Derm Venereol. 2017;97(4):532–533. doi: 10.2340/00015555-2549.
40. Bitoun E, Chavanas S, Irvine AD, et al. Netherton syndrome: disease expression and spectrum of SPINK5 mutations in 21 families. J Invest Dermatol. 2002;118(2):352–361. doi: 10.1046/j.15231747.2002.01603.x.
41. Deraison C, Bonnart C, Lopez F, et al. LEKTI fragments specifically inhibit KLK5, KLK7, and KLK14 and control desquamation through a pH-dependent interaction. Mol Biol Cell. 2007;18(9):3607–3619. doi: 10.1091/mbc.e07-02-0124.
42. Briot A, Deraison C, Lacroix M, et al. Kallikrein 5 induces atopic dermatitis-like lesions through PAR2-mediated thymic stromal lymphopoietin expression in Netherton syndrome. J Exp Med. 2009;206(5):1135–1147. doi: 10.1084/jem.20082242.
43. Oji V, Eckl KM, Aufenvenne K, et al. Loss of corneodesmosin leads to severe skin barrier defect, pruritus, and atopy: unraveling the peeling skin disease. Am J Hum Genet. 2010;87(2):274–281. doi: 10.1016/j.ajhg.2010.07.005.
44. Israeli S, Zamir H, Sarig O, et al. Inflammatory peeling skin syndrome caused by a mutation in CDSN encoding corneodesmosin. J Invest Dermatol. 2011;131(3):779–781. doi: 10.1038/jid.2010.363.
45. Samuelov L, Sarig O, Harmon RM, et al. Desmoglein 1 deficiency results in severe dermatitis, multiple allergies and metabolic wasting. Nat Genet. 2013;45(10):1244–1248. doi: 10.1038/ng.2739.
46. McAleer MA, Pohler E, Smith FJ, et al. Severe dermatitis, multiple allergies, and metabolic wasting syndrome caused by a novel mutation in the N-terminal plakin domain of desmoplakin. J Allergy Clin Immunol. 2015;136(5):1268–1276. doi: 10.1016/j.jaci.2015.05.002.
47. Fine JD, Eady RA, Bauer EA, et al. The classification of inherited epidermolysis bullosa (EB): Report of the Third International Consensus Meeting on Diagnosis and Classification of EB. J Am Acad Dermatol. 2008;58(6):931–950. doi: 10.1016/j.jaad.2008.02.004.
48. Shinkuma S. Dystrophic epidermolysis bullosa: a review. Clin Cosmet Investig Dermatol. 2015;8:275–284. doi: 10.2147/CCID.S54681.
49. Makarova SG, Namazova-Baranova LS, Murashkin NN, et al. Food allergy in children with inherited epidermolysis bullosa. the results of the observational study. Annals of the Russian Academy of Medical Sciences. 2018;73(1):49–58. (In Russ). doi: 10.15690/vramn847.
Review
For citations:
Murashkin N.N., Ivanov R.A., Savelova A.A., Fedorov D.V., Opryatin L.A., Ahmad W. Role of the Epidermal Barrier in the Formation of Food Allergies in Children with Genodermatosis. Pediatric pharmacology. 2019;16(4):234-240. (In Russ.) https://doi.org/10.15690/pf.v16i4.2053
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