Table 2.

Summary of microbiome studies

Author	Disease studied	Skin site	Number patients
				Method	Results
Frank et al 20031	normal	outer ear canal	24	RFLP; Sanger sequencing	45 spp; microbial community complexity greater in males and older individuals; species composition correlated with consanguinity but not with household association
Dekio et al 20052	normal	forehead	5	16S rRNA gene sequencing	32 OTUs; 62% sequences P. acnes; 9 species previously not known to live on skin
Gao et al 20073	normal	volar forearm	6 (4 resampled 8–10 mos later)	16S rRNA gene sequencing	182 OTUs; 19% sequences Proteobacteria, 51% Actinobacteria, 24% Firmicutes; 63% of sequences common to all subjects; 54% common to both time points; 50–77% identity between R and L arms
Grice et al 20084	normal	antecubital fossa	6 (4 resampled 8–10 mos later)	skin swab, scrape, or punch biopsy; 16S rRNA gene sequencing	113 OTUs; swab, scrape, and punch gave similar results; >90% Proteobacteria (Pseudomonas spp predominant)
Fierer et al 20085	normal	palm	51	16S rRNA gene sequencing	4,742 OTUs; 32% sequences Propionibacterium, 17% Streptococcus, 8% Staphylococcus; 17% identity between R and L hands; 13% identity between individuals; greater diversity in female hands
Grice et al 20096	normal	20 skin sites	10 (5 resampled 4–6 mos later)	16S rRNA gene sequencing	Similar habitats (moist, sebaceous, or dry) had similar microbial compositions; Outer ear and nares were most stable over time; Popliteal fossae, arms, buttocks least stable over time
Costello et al 20097	normal	18 skin sites	9 (resampled 4 times in 3 mos)	16S rRNA gene sequencing	Same habitats are similar between individuals; Inoculation of habitat with bacteria from another site did not significantly change microbiota over time
Dominguez-Bello et al 20108	normal newborn	forearm, forehead	10 newborns, 9 mothers	16S rRNA gene sequencing	Newborns are homogenously colonized; Microbial composition dependent on delivery mode (C-section versus vaginal delivery)
Capone et al 20119	normal infant	volar forearm, buttock, forehead	31 infants age 3 to 52 wks; 5 mothers	16S rRNA gene sequencing	Diversity "evenness" increases with age; Staph and Strep spp decrease in relative abundance with age. Bacilli, Clostridia, Actinobacteria are most frequent classes in infant skin.
Oh et al 201210	normal child and adult	nares, volar forearm, antecubital fossa, popliteal fossa,	28 individuals, age 2–40 yrs	16S rRNA gene sequencing	Microbial diversity of nares increases with sexual maturity. Dominant phyla across all skin sites differed globally between children and adults. S. aureus was overrepresented in nares of younger children and correlated to presence at other skin sites.
Bek-Thomsen et al 200811	acne	facial folicle, cheek	5 pts (not on therapy), 3 normal	16S rRNA gene sequencing	30 OTUs; Healthy follicles contained only P. acnes; Acne follicles had 53–92% P. acnes but also had other bacteria
Price et al 200912	chronic wounds	wound	24 pts	16S rRNA gene sequencing from wound cultures	Recent antibiotics changes wound microbiota, increases Pseudomonadaceae; Diabetic wounds have increased Streptococcaceae
Gontcharova et al 201013	diabetic ulcers	wound and contralateral normal skin	23 wound, 28 normal	16S rRNA gene sequencing	Wounds less diverse than intact skin; Wounds have more Corynebacteriaceae, Streptococcaceae, and anaerobes; Intact skin and wound on same individual do not have more related microbiomes
Paulino et al 200614	psoriasis	plaque, forearm	3 pts, 5 normal	18s rRNA gene sequencing	No significant difference in Malassezia populations in healthy versus psoriatic skin
Gao et al 200815	psoriasis	plaque	6 pts	16S rRNA gene sequencing	Psoriatic plaques have more Firmicutes (39% vs 24% in normal skin)
Fahlen et al 201216	psoriasis	plaque biopsy	10 pts, 12 normal	16S rRNA gene sequencing	652 OTUs; Psoriatic plaques have more Streptococcus, similar levels of Firmicutes
Sugita et al 200117	AD	scalp, back, nares	32 pts (on topical steroids), 18 healthy	IGS gene sequencing	AD pts have different composition of Malasseiza species with more M. globosa, M. restricta, and M. furfur
Sugita et al 200418	AD		13 AD, 12 normal	IGS gene sequencing	Different strains of M. restricta in AD versus normal skin
Dekio et al 200719	AD	face	13 AD, 10 normal	16S rRNA RFLP analysis	18 species; Stenotophomonas maltophilia most common colonizer of AD skin; S. aureus not seen in any samples
Kong et al 201220	AD	antecubital fossa, popliteal fossa, forearm, nare	12 AD, 11 healthy	16S rRNA gene sequencing	AD flares characterized by 65% increase in Staphylococcus spp, predominantly S. aureus and S. epidermidis; AD flares while on intermittent treatment only 15% slight increase in Staphylococcus colonization; Complete treatment of flares re-diversified microbiome

Abbreviations: AD = atopic dermatitis, OTU = operational taxonomic unit, pts = patients, mos = months, spp = species

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^3.Gao Z, Tseng CH, Pei Z , Blaser MJ. Molecular analysis of human forearm superficial skin bacterial biota. Proceedings of the National Academy of Sciences of the United States of America 2007;104:2927-32.

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^11.Bek-Thomsen M, Lomholt HB, Kilian M. Acne is not associated with yet-uncultured bacteria. Journal of clinical microbiology 2008;46:3355-60.

^12.Price LB, Liu CM, Melendez JH, Frankel YM, Engelthaler D, Aziz M et al. Community analysis of chronic wound bacteria using 16S rRNA gene-based pyrosequencing: impact of diabetes and antibiotics on chronic wound microbiota. PloS one 2009;4:e6462.

^13.Gontcharova V, Youn E, Sun Y, Wolcott RD, Dowd SE. A comparison of bacterial composition in diabetic ulcers and contralateral intact skin. The open microbiology journal 2010;4:8-19.

^14.Paulino LC, Tseng CH, Strober BE, Blaser MJ. Molecular analysis of fungal microbiota in samples from healthy human skin and psoriatic lesions. Journal of clinical microbiology 2006;44:2933-41.

^15.Gao Z, Tseng CH, Strober BE, Pei Z, Blaser MJ. Substantial alterations of the cutaneous bacterial biota in psoriatic lesions. PloS one 2008;3:e2719.

^16.Fahlen A, Engstrand L, Baker BS, Powles A, Fry L. Comparison of bacterial microbiota in skin biopsies from normal and psoriatic skin. Archives of dermatological research 2012;304:15-22.

^17.Sugita T, Suto H, Unno T, Tsuboi R, Ogawa H, Shinoda T et al. Molecular analysis of Malassezia microflora on the skin of atopic dermatitis patients and healthy subjects. Journal of clinical microbiology 2001;39:3486-90.

^18.Sugita T, Tajima M, Amaya M, Tsuboi R, Nishikawa A. Genotype analysis of Malassezia restricta as the major cutaneous flora in patients with atopic dermatitis and healthy subjects. Microbiology and immunology 2004;48:755-9.

^19.Dekio I, Sakamoto M, Hayashi H, Amagai M, Suematsu M, Benno Y. Characterization of skin microbiota in patients with atopic dermatitis and in normal subjects using 16S rRNA gene-based comprehensive analysis. Journal of medical microbiology 2007;56:1675-83.

^20.Kong HH, Oh J, Deming C, Conlan S, Grice EA, Beatson MA et al. Temporal shifts in the skin microbiome associated with disease flares and treatment in children with atopic dermatitis. Genome research 2012;22:850-9.