TY - JOUR
T1 - Skin microbiome prior to development of atopic dermatitis
T2 - early colonization with commensal staphylococci at 2 months is associated with a lower risk of atopic dermatitis at 1 year
AU - Kennedy, Elizabeth A
AU - Connolly, Jennifer
AU - O.'B. Hourihane, Jonathan
AU - Fallon, Padraic G.
AU - McLean, W. H. Irwin
AU - Murray, Deirdre
AU - Jo, Jay-Hyun
AU - Segre, Julia A.
AU - Kong, Heidi H.
AU - Irvine, Alan D.
N1 - Open Access funded by Wellcome Trust.
PY - 2017/1
Y1 - 2017/1
N2 - Background: Disease flares of established atopic dermatitis (AD) are generally associated with a low-diversity skin microbiota and Staphylococcus aureus dominance. The temporal transition of the skin microbiome between early infancy and the dysbiosis of established AD is unknown.Methods: We randomly selected 50 children from the Cork BASELINE longitudinal birth cohort for microbiome sampling at three times in the first six months of life, at four skin sites relevant to AD: the antecubital and popliteal fossae, nasal tip, and cheek. We identified ten infants who developed AD and compared them with ten randomly selected control infants with no AD. We performed bacterial 16S ribosomal RNA sequencing and analysis directly from clinical samples.Results: Bacterial community structures and diversity shifted over time, suggesting that age strongly affects the skin microbiome in infants. Unlike established AD, these infantile AD patients did not have noticeably dysbiotic communities prior to or with disease and were not colonized by S. aureus. In comparing patients and controls, infants who had affected skin at month 12 had statistically significant differences in bacterial communities on the antecubital fossa at month 2 compared to infants who were unaffected at month 12. In particular, commensal staphylococci were significantly less abundant in infants affected at month 12, suggesting that this genus may protect against the later development of AD.Conclusions: This study suggests that 12-month-old infants with AD were not colonized with Staphylococcus aureus before developing AD. Additional studies are needed to confirm if colonization with commensal staphylococci modulates skin immunity and attenuates development of AD.
AB - Background: Disease flares of established atopic dermatitis (AD) are generally associated with a low-diversity skin microbiota and Staphylococcus aureus dominance. The temporal transition of the skin microbiome between early infancy and the dysbiosis of established AD is unknown.Methods: We randomly selected 50 children from the Cork BASELINE longitudinal birth cohort for microbiome sampling at three times in the first six months of life, at four skin sites relevant to AD: the antecubital and popliteal fossae, nasal tip, and cheek. We identified ten infants who developed AD and compared them with ten randomly selected control infants with no AD. We performed bacterial 16S ribosomal RNA sequencing and analysis directly from clinical samples.Results: Bacterial community structures and diversity shifted over time, suggesting that age strongly affects the skin microbiome in infants. Unlike established AD, these infantile AD patients did not have noticeably dysbiotic communities prior to or with disease and were not colonized by S. aureus. In comparing patients and controls, infants who had affected skin at month 12 had statistically significant differences in bacterial communities on the antecubital fossa at month 2 compared to infants who were unaffected at month 12. In particular, commensal staphylococci were significantly less abundant in infants affected at month 12, suggesting that this genus may protect against the later development of AD.Conclusions: This study suggests that 12-month-old infants with AD were not colonized with Staphylococcus aureus before developing AD. Additional studies are needed to confirm if colonization with commensal staphylococci modulates skin immunity and attenuates development of AD.
KW - Staphylococcus aureus
KW - Atopic dermatitis
KW - Skin
KW - microbiome
KW - Longitudinal birth cohort
KW - 16S sequencing
U2 - 10.1016/j.jaci.2016.07.029
DO - 10.1016/j.jaci.2016.07.029
M3 - Article
C2 - 27609659
SN - 0091-6749
VL - 139
SP - 1
EP - 7
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
IS - 1
M1 - 166-172
ER -