Altered skin microbiome: The most important symptom of atopic dermatitis

Cover Page


Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

The progressively increased incidence of atopic dermatitis among children and increased persistence in adulthood, combined with an inevitably decreased quality of life of patients, determine the relevance of studying the development mechanisms of this disease not only for dermatology but also for the entire health care system. Thus, the prerequisites for the emergence of new pathogenetic concepts and the search for the most effective therapeutic modalities arise. Currently, atopic dermatitis is considered as the interaction of endogenous (impaired immune response and insufficient epidermal barrier function) and exogenous (exposure to allergens, chemical or physical irritants, and microorganisms) factors.

Environmental factors, such as temperature and humidity, genetic makeup, antibiotic use, and good hygiene, play a critical role in skin microbiome maintenance and stability. Normally, the skin microbiota is mainly formed by bacteria of the genus Staphylococcus, Propionibacterium, Corynebacterium, and Streptococcus. In 70% of patients with atopic dermatitis, colonization of Staphylococcus aureus is observed on the affected skin, whereas on the unaffected skin in 39%, which secondarily contributes to the development of immune imbalance and increased skin xerosis. This fact determines the importance of basic therapy, which, on one hand, helps to strengthen the epidermal barrier, and on the other, normalizes the microbiome of the skin, thereby reducing the colonization of Staphylococcus aureus.

The normal skin microbiome suppresses the activity of immune-inflammatory responses and regulates pH, lipid synthesis, and transepidermal water loss. Thus, skin microbiome normalization is the key to successful therapy and long-term remission of atopic dermatitis.

Full Text

Restricted Access

About the authors

Olga B. Tamrazova

Moscow’s Healthcare Department Children Hospital of Z.A. Bashlyaeva; Peoples’ Friendship University of Russia

Email: anait_tamrazova@mail.ru
ORCID iD: 0000-0003-3261-6718
SPIN-code: 5476-8497

MD, Dr. Sci. (Med), Professor

Russian Federation, 28, Geroev Panfilovcev street, Moscow, 125373; Moscow

Evgeniya A. Glukhova

Moscow’s Healthcare Department Children Hospital of Z.A. Bashlyaeva; Federal Research Center of Nutrition and Biotechnology

Email: evgeniya.shmeleva1994@yandex.ru
ORCID iD: 0000-0002-3004-6646
Russian Federation, 28, Geroev Panfilovcev street, Moscow, 125373; Moscow

Anait V. Tamrazova

Central State Medical Academy of Department of Presidential Affairs; Krasnogorsk Dermatovenerologic Dispensary

Email: anaittamrazova@gmail.com
ORCID iD: 0000-0002-4672-697X
SPIN-code: 1563-1190

 

 
Russian Federation, Moscow; Krasnogorsk

Natalia F. Dubovets

Moscow’s Healthcare Department Children Hospital of Z.A. Bashlyaeva

Author for correspondence.
Email: skorpionka_n@mail.ru
ORCID iD: 0000-0003-3278-4797
SPIN-code: 3677-5969
Russian Federation, 28, Geroev Panfilovcev street, Moscow, 125373

References

  1. Frazier W, Bhardwaj N. Atopic dermatitis: diagnosis and treatment. Am Fam Physician. 2020;101(10):590–598.
  2. Bylund S, Kobyletzki LB, Svalstedt M, Svensson А. Prevalence and incidence of atopic dermatitis: a systematic review. Acta Derm Venereol. 2020;100(12):adv00160. doi: 10.2340/00015555-3510
  3. Nutten S. Atopic dermatitis: global epidemiology and risk factors. Ann Nutr Metab. 2015;66(Suppl 1):8–16. doi: 10.1159/000370220
  4. Williams H, Stewart A, von Mutius E, et al. International Study of Asthma and Allergies in Childhood (ISAAC) Phase One and Three Study Groups. Is eczema really on the increase worldwide? J Allergy Clin Immunol. 2008;121(4):947–954.e15. doi: 10.1016/j.jaci.2007.11.004
  5. De la O-Escamilla NO, Sidbury R. Atopic dermatitis: update on pathogenesis and therapy. Pediatr Ann. 2020;49(3):e140–e146. doi: 10.3928/19382359-20200217-01
  6. Brandner JM. Importance of tight junctions in relation to skin barrier function. Curr Probl Dermatol. 2016;49:27–37. doi: 10.1159/000441541
  7. Sanford JA, Gallo RL. Functions of the skin microbiota in health and disease. Semin Immunol. 2013;25(5):370–377. doi: 10.1016/j.smim.2013.09.005
  8. Edslev SM, Agner T, Andersen PS. Skin microbiome in atopic dermatitis. Acta Derm Venereol. 2020;100(12):adv00164. doi: 10.2340/00015555-3514
  9. Marchionini A, Hausknecht W. Sauremantel der haut und bakterienabwehr. I. Mitteilung. Die regionare verschiedenheit der wasserstoffionenkonzentration der hautoberflache. Klin Wochenschr. 1938;17:663–666.
  10. Verdier-Sévrain S, Bonté F. Skin hydration: a review on its molecular mechanisms. J Cosmet Dermatol. 2007;6(2):75–82. doi: 10.1111/j.1473-2165.2007.00300.x
  11. Nouwen AE, Karadavut D, Pasmans SG, et al. Natural moisturizing factor as a clinical marker in atopic dermatitis. Allergy. 2020;75(1):188–190. doi: 10.1111/all.13942
  12. Oh J, Byrd AL, Deming C, et al. Biogeography and individuality shape function in the human skin metagenome. Nature. 2014;514(7520):59–64. doi: 10.1038/nature13786
  13. Clausen ML, Agner T, Lilje B, et al. Association of disease severity with skin microbiome and filaggrin gene mutations in adult atopic dermatitis. JAMA Dermatol. 2018;154(3):293–300. doi: 10.1001/jamadermatol.2017.5440
  14. Oh J, Byrd AL, Park M; NISC Comparative Sequencing Program. Temporal stability of the human skin microbiome. Cell. 2016;165(4):854–866. doi: 10.1016/j.cell.2016.04.008
  15. 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
  16. Blicharz L, Rudnicka L, Czuwara J, et al. The influence of microbiome dysbiosis and bacterial biofilms on epidermal barrier function in atopic dermatitis-an update. Int J Mol Sci. 2021;22(16):8403. doi: 10.3390/ijms22168403
  17. Byrd AL, Belkaid Y, Segre JA. The human skin microbiome. Nat Rev Microbiol. 2018;16(3):143–155. doi: 10.1038/nrmicro.2017.157
  18. Leyden JJ, Marples RR, Kligman AM. Staphylococcus aureus in the lesions of atopic dermatitis. Br J Dermatol. 1974;90(5):525–530. doi: 10.1111/j.1365-2133.1974.tb06447.x
  19. Di Domenico EG, Cavallo I, Capitanio B, et al. Staphylococcus aureus and the cutaneous microbiota biofilms in the pathogenesis of atopic dermatitis. Microorganisms. 2019;7(9):301. doi: 10.3390/microorganisms7090301
  20. Totté JE, van der Feltz WT, Hennekam M, et al. Prevalence and odds of Staphylococcus aureus carriage in atopic dermatitis: a systematic review and meta-analysis. Br J Dermatol. 2016;175(4):687–695. doi: 10.1111/bjd.14566
  21. Cabanillas B, Novak N. Atopic dermatitis and filaggrin. Curr Opin Immunol. 2016;42:1–8. doi: 10.1016/j.coi.2016.05.002
  22. Visser MJ, Landeck L, Campbell LE, et al. Impact of atopic dermatitis and loss-of-function mutations in the filaggrin gene on the development of occupational irritant contact dermatitis. Br J Dermatol. 2013;168(2):326–332. doi: 10.1111/bjd.12083
  23. Miajlovic H, Fallon PG, Irvine AD, Foster TJ. Effect of filaggrin breakdown products on growth of and protein expression by Staphylococcus aureus. J Allergy Clin Immunol. 2010;126:1184–1190.e3.
  24. Fleury OM, McAleer MA, Feuillie C, et al. Clumping factor B promotes adherence of Staphylococcus aureus to corneocytes in atopic dermatitis. Infect Immun. 2017;85(6):e00994-16. doi: 10.1128/IAI.00994-16
  25. Kim BS, Choi JK, Jung HJ, et al. Effects of topical application of a recombinant staphylococcal enterotoxin A on DNCB and dust mite extract-induced atopic dermatitis-like lesions in a murine model. Eur J Dermatol. 2014;24(2):186–193. doi: 10.1684/ejd.2014.2302
  26. Simon M. Effects of environmental skin stressors on filaggrin degradation products: importance for eczema. Br J Dermatol. 2018;179(3):560–561. doi: 10.1111/bjd.16822
  27. Nakatsuji T, Chen TH, Two AM, et al. Staphylococcus aureus exploits epidermal barrier defects in atopic dermatitis to trigger cytokine expression. J Invest Dermatol. 2016;136(11):2192–2200. doi: 10.1016/j.jid.2016.05.127
  28. Brandner JM, Zorn-Kruppa M, Yoshida T, et al. Epidermal tight junctions in health and disease. Tissue Barriers. 2015;3(1-2):e974451. doi: 10.4161/21688370.2014.974451
  29. Ohnemus U, Kohrmeyer K, Houdek P, et al. Regulation of epidermal tight-junctions (TJ) during infection with exfoliative toxin-negative Staphylococcus strains. J Invest Dermatol. 2008;128(4):906–916. doi: 10.1038/sj.jid.5701070
  30. Nakamura Y, Oscherwitz J, Cease KB, et al. Staphylococcus δ-toxin induces allergic skin disease by activating mast cells. Nature. 2013;503(7476):397–401. doi: 10.1038/nature12655
  31. Otto M. Staphylococcal biofilms. Curr Top Microbiol Immunol. 2008;322:207–228. doi: 10.1007/978-3-540-75418-3_10
  32. Flemming HC, Wingender J, Szewzyk U, et al. Biofilms: an emergent form of bacterial life. Nat Rev Microbiol. 2016;14(9):563–575. doi: 10.1038/nrmicro.2016.94
  33. Verallo-Rowell VM, Dillague KM, Syah-Tjundawan BS. Novel antibacterial and emollient effects of coconut and virgin olive oils in adult atopic dermatitis. Dermatitis. 2008;19(6):308–315.
  34. Glatz M, Jo JH, Kennedy EA, et al. Emollient use alters skin barrier and microbes in infants at risk for developing atopic dermatitis. PLoS One. 2018;13(2):e0192443. doi: 10.1371/journal.pone.0192443
  35. Wollenberg A, Barbarot S, Bieber T, et al. Consensus-based European guidelines for treatment of atopic eczema (atopic dermatitis) in adults and children: part I [published correction appears in J Eur Acad Dermatol Venereol. 2019;33(7):1436]. J Eur Acad Dermatol Venereol. 2018;32(5):657–682. doi: 10.1111/jdv.14891
  36. Gueniche A, Knaudt B, Schuck E, et al. Effects of nonpathogenic gram-negative bacterium Vitreoscilla filiformis lysate on atopic dermatitis: a prospective, randomized, double-blind, placebo-controlled clinical study. Br J Dermatol. 2008;159(6):1357–1363. doi: 10.1111/j.1365-2133.2008.08836.x
  37. Seité S, Zelenkova H, Martin R. Clinical efficacy of emollients in atopic dermatitis patients ― relationship with the skin microbiota modification. Clin Cosmet Investig Dermatol. 2017;10:25–33. doi: 10.2147/CCID.S121910

Supplementary files

Supplementary Files
Action
1. Fig. 1. Patient A., 4 years old. Atopic dermatitis, erythematous-squamous form, secondary infection. Signs of secondary infection: increased itching and weeping, cracks, hemorrhagic crusts.

Download (127KB)
Indexing metadata
2. Fig. 2. Patient G., 3 years old. Atopic dermatitis, stage of incomplete remission, skin xerosis. Nummular (microbial) eczema. Signs of secondary infection: yellow crusts against a background of pale pink erythema with clear oval-shaped borders.

Download (99KB)
Indexing metadata
3. Fig. 3. Patient M., 12 years old. Atopic dermatitis, stage of incomplete remission, skin xerosis. A common secondary infection. Signs of secondary infection: peeling, increased itching.

Download (132KB)
Indexing metadata

Copyright © Pharmarus Print Media, 2021



This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies