Barrier Function and Microbiotic Dysbiosis in Atopic Dermatitis. Mike Levin Division of asthma and allergy Department of paediatrics
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1 Barrier Function and Microbiotic Dysbiosis in Atopic Dermatitis Mike Levin Division of asthma and allergy Department of paediatrics
2 Eczema / dermatitis is an inflammatory skin reaction
3 Atopic Phototoxic Contact Dermatitis Photoallergic Seborrhoeic Irritant
4 Aetiopathogenesis Genetics Atopy Skin barrier disruption Environmental irritants Environmental allergens Microbes
5 Leung 2014 JACI
6 Allergist Dermatologist Eczema is an allergy. No, it s a skin condition.
7 Outside-inside / Inside-outside Outside inside hypothesis Xerosis and abnormal permeability of skin barrier drives eczema with secondary sensitisation Inside outside hypothesis Inflammatory responses to irritants and allergens drives eczema with secondary barrier disruption:
8 T cells in skin lesions of atopic dermatitis
9 Atopic eczema: A skin barrier disease
10 The brick wall model of the skin barrier Bricks : cells (corneocytes) Iron rods : hold cells together (corneodesmosomes) Cement : around the cells (lipid lamellae)
11 The brick wall model of the skin barrier
12 Fillagrin - Profillaggrin cleaved to fillagrin - Fillagrin aggregates the keratin skeleton and causes flattening - Filaggrin proteolysed into natural moisturising factor and acidifies the surface - Protects against Staph toxin induced keratinocyte death - Mutations cause dryness - Early onset AD - More persistent AD - Association with asthma, FA and infection - Enhanced expression of IL1 cytokines
13 Tight junctions on stratum Normal skin granulosum keratinocytes Atopic dermatitis De Benedetto JACI
14 Others - Filaggrin-2 - Hornerin - SPINK 5 gene (Serine protease inhibitor Kazal type 5) - Encodes the protease inhibitor lymphoepithelial Kazal-typerelated inhibitor (LEKTI) - Regulates desquamation - SPRR3 small proline rich protein 3
15 The brick wall model of the skin barrier Skin barrier breakdown in atopic dermatitis
16 The brick wall model of the skin barrier Portal of entry IRRITANTS ALLERGENS
17 Complexity: Interrelationships! Eczema as an entry point for allergens Intact skin Broken skin Stratum corneum Epidermis Dermis Subcutaneous tissue Systemic circulation
18 Atopy Barrier Atopic dermatitis
19 Atopy Allergen Barrier Dry skin Pruritis Irritants Atopic dermatitis Infection Lesions
20 Leung 2014 JACI
21 Leung 2014 JACI
22 Leung 2014 JACI
23 Leung 2014 JACI
24 Phases of Atopic Dermatitis Irritants Allergens Scratching tissue damage Nonatopic dermatitis Sensitisation to allergens Atopic dermatitis Sensitisation to self proteins Auto-allergic dermatitis Impaired epidermal barrier Receptors, cytokines etc Tissue-related genes Atopic genes (cytokines receptors) Genes
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29 Normal Skin Actinobacteria Corynebacterium Propionibacterium Rothia Actinomyces Bacteroidetes Prevotella Proteobacteria Alphaproteobacteria Betaproteobacteria Gammaproteobacteria Firmicutes Streptococcus Staphylococcus Granulicatella
30 Normal Skin Actinobacteria Corynebacterium Propionibacterium Rothia Actinomyces Bacteroidetes Prevotella Proteobacteria Alphaproteobacteria Betaproteobacteria Gammaproteobacteria Firmicutes Streptococcus Staphylococcus Granulicatella Lesional skin Decreased Corynebacterium No change Decreased Alphaproteobacteria Increased Staphylococcus, Decreased Streptococcus, Granulicatella
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32 Increased Staph at baseline and worse during flare. Kong et al Genome res
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35 Atopy Genes Dysbiosis Infecton Itch
36 Atopy Immune dysfunction Genes Barrier dysfunction Dysbiosis Irritants Infection Itch
37 Atopy Immune dysfunction Genes Barrier dysfunction Dysbiosis Irritants Infection Itch
38 Atopy Immune dysfunction Genes Barrier dysfunction Dysbiosis Irritants Infection Itch
39 HBD-2 immunostaining LL-37 immunostaining Endogenous antimicrobial peptides decreased Ong 2002 NEJM
40 Atopy Immune dysfunction Genes Barrier dysfunction Staph Irritants Infection Itch
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42 Mast cells stimulated with Delta toxin degranulate Delta toxin causes skin disease Nakumura 2013 Nature
43 Staphylococcal extracts
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46 Increased Staph at baseline and worse during flare Causes marked loss of diversity Kong et al Genome res
47 Kong et al Genome res
48 Microbial diversity Normal Atopic dermatitis Salava 2014 CTA
49 Kong et al Genome res
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52 Without With S Epi S Epi Lai 2009 Nature med
53 Therapeutic implications
54 Blah Blah Random fact Whatever Some mechanism Cycle Side issue Cause Effect
55 Severity Phases and treatment of Atopic Dermatitis Flare Flare Skin with acute flare-ups Acute phases (flareups): Topical steroids Interval Subclinical inflammation Time Interval Interval phases Interval (non-acute) phases: Emollient treatments
56 Restore skin barrier Avoid triggers and aggravators Avoid soap Use bath oils and wash with soap substitute: cleansing oils or creams Moisturize use a good emollient at least twice a day
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60 Wet Dressings Reduce the itch Cooling and soothing Moisturise the skin Protect the skin Help skin heal
61 Before emollients Affected skin Unaffected skin Staph Staph After 2 ½ months emollients Corynebacterium Xanthomonas Staphylococcus Unassigned Propionibacterium Alicyclobacillus Acinetobacter Micrococcus Wautersiella Enhydrobacter Streptococcus Genera_unassigned Finegoldia Prevotella Brevibacterium Paracoccus Peptoniphilus Anaerococcus Affected skin Staph Unaffected skin Staph Seite et al J drugs dermatol
62 Unaffected skin before emollient Unaffected skin after emollient Affected skin before emollient Affected skin after emollient Other Staphylococcus Staphylococcus Staphylococcus Staphylococcus Staphylococcacea spp aureus epidermidis haemolyticus
63 Anti-Staph approach Bleach baths Nasal eradication Topical antibiotics
64 Future strategies? Direct manipulation of microbiome Apply bacterial products to skin
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