Atopic dermatitis microbiomes stratify into ecologic dermotypes enabling microbial virulence and disease severity

Atopic dermatitis (AD) is an inflammatory dermatosis with a pathogenesis believed to be due to a combination of genetic, immunologic and environmental factors that affects up to 5% of adults and 20% of children worldwide. 1,2 Common genetic factors include polymorphisms in the filaggrin structural protein, interleukin (IL)-4 receptor and vitamin D receptor. [3][4][5] AD is driven by multiple immune pathways, most commonly with activation of Th2 and Th22 T-cell subsets. 6 Crosstalk between commensals and the host immune system modulates adaptive and innate immune responses in AD. 7 Staphylococcus aureus (SA) in AD lesions and surrounding normal skin was first noted by Leyden et al. in the 1970s; since then, the understanding of its role in AD has drastically evolved. 8,9 SA is a well-established exacerbator of AD; it is frequently isolated from the skin of AD patients and increased SA density is found during flares. 10 A meta-analysis in 2016 reported a pooled prevalence of SA colonization among AD patients of 70% in lesional skin, 39% in non-lesional skin and 62% in the nose. 11 More recently, Kong et al 12 found that AD treatments and flares were closely associated with shifts in the cutaneous microbial diversity. While current evidence has established that SA proliferates during flares and plays a role in the cycle of epidermal breakdown and inflammation, a true causal relationship has not been established. Herein, we will summarize the

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“…with abundance of Staphylococcal spp. 78 These studies support the growing hypothesis that commensals are important in maintaining healthy skin.…”

Section: Sa Interacts With Host Commensalssupporting

confidence: 63%

Updated understanding of Staphylococcus aureus in atopic dermatitis: From virulence factors to commensals and clonal complexes

Hwang

Thompson

Jaros

et al. 2021

Experimental Dermatology

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“…Delftia acidovorans, a gram-negative bacterium, is detected in the skin of AD patients by microbiome analysis [18][19][20][21][22]. D. acidovorans secretes a compound with antimicrobial activity against S. aureus, Enterococcus faecalis, Acinetobacter baumannii, Klebsiella pneumoniae, and Pseudomonas aeruginosa [23].…”

Section: Introductionmentioning

confidence: 99%

Delftia acidovorans secretes substances that inhibit the growth of Staphylococcus epidermidis through TCA cycle-triggered ROS production

et al. 2021

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The proportion of Staphylococcus aureus in the skin microbiome is associated with the severity of inflammation in the skin disease atopic dermatitis. Staphylococcus epidermidis, a commensal skin bacterium, inhibits the growth of S. aureus in the skin. Therefore, the balance between S. epidermidis and S. aureus in the skin microbiome is important for maintaining healthy skin. In the present study, we demonstrated that the heat-treated culture supernatant of Delftia acidovorans, a member of the skin microbiome, inhibits the growth of S. epidermidis, but not that of S. aureus. Comprehensive gene expression analysis by RNA sequencing revealed that culture supernatant of D. acidovorans increased the expression of genes related to glycolysis and the tricarboxylic acid cycle (TCA) cycle in S. epidermidis. Malonate, an inhibitor of succinate dehydrogenase in the TCA cycle, suppressed the inhibitory effect of the heat-treated culture supernatant of D. acidovorans on the growth of S. epidermidis. Reactive oxygen species production in S. epidermidis was induced by the heat-treated culture supernatant of D. acidovorans and suppressed by malonate. Further, the inhibitory effect of the heat-treated culture supernatant of D. acidovorans on the growth of S. epidermidis was suppressed by N-acetyl-L-cysteine, a free radical scavenger. These findings suggest that heat-resistant substances secreted by D. acidovorans inhibit the growth of S. epidermidis by inducing the production of reactive oxygen species via the TCA cycle.

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“…However, other CoNS such as S. epidermidis and S. hominis were enriched in the dermotype B. Interestingly this pathologic dermotype was also enriched for staphylococcal virulence genes and correlated with disease severity and itch intensity. 58 Further analyses of specific S. aureus strains of AD patients over time are needed to classify the characteristics of AD strains in order to discover the distinct markers of AD-derived S. aureus.…”

Section: S Taphylococcus Aureus S K I N Coloniz Ati On and Atopi C Dermatitismentioning

confidence: 99%

Beneficial effects of coagulase‐negative Staphylococci on Staphylococcus aureus skin colonization

Bier

Schittek

2021

Experimental Dermatology

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Our body contains an estimated composition of 10 10 microbes on the skin. 1 Among the most common colonizers are corynebacteria, cutibacteria and coagulase-negative staphylococci (CoNS). [2][3][4] The different skin sites provide distinct microenvironments that shape the composition of the local microbiota: while sebaceous sites display a low diversity in microbe composition and are dominated by lipophilic cutibacteria, moist skin sites are colonized by a diverse set of staphylococci, corynebacteria and micrococci. 3 Interestingly, dry skin sites exhibit the most diverse microbiome composition and are colonized by cutibacteria, staphylococci, corynebacteria, streptococci and micrococci. In contrast to the bacterial microbiome, the composition of the fungal microbiome is largely dominated by Malassezia species and not determined by the body-site. [5][6][7] The composition of the skin microbiome in newborns was shown to be diverse across different body sites and initially depends on the delivery mode. 8 When comparing the microbiome on axillary skin between the different birth modes, S. epidermidis, S. hominis and E. coli prevalence was significantly lower in caesarean-than in vaginallyborn infants at birth. S. lugdunensis, however, was detected in some of caesarean-but not in vaginally-born children. In this study, birth mode-related differences in skin colonization were no longer detectable at 1 week of age except for E. coli, prevalence of which became similar in all children at 3 months of age. 9 In conclusion, site specificity is established already within the first days after birth 9,10 and

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Atopic dermatitis microbiomes stratify into ecologic dermotypes enabling microbial virulence and disease severity

Cited by 35 publications

References 55 publications

Updated understanding of Staphylococcus aureus in atopic dermatitis: From virulence factors to commensals and clonal complexes

Updated understanding of Staphylococcus aureus in atopic dermatitis: From virulence factors to commensals and clonal complexes

Delftia acidovorans secretes substances that inhibit the growth of Staphylococcus epidermidis through TCA cycle-triggered ROS production

Beneficial effects of coagulase‐negative Staphylococci on Staphylococcus aureus skin colonization

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