Staphylococcus aureus colonization in atopic eczema and its association with filaggrin gene mutations.
BACKGROUND
Atopic dermatitis (AD) is a prevalent disease with significant impact on physical health and quality of life. Staphylococcus aureus has been directly correlated to disease severity, and may also be a contributing causal factor in the pathogenesis of AD.


OBJECTIVE
The primary aim was to assess differences in S. aureus colonization in patients with AD with and without filaggrin gene mutations. The secondary aim was to assess disease severity in relation to S. aureus colonization. Exploratory analyses were performed to investigate S. aureus genetic lineages in relation to filaggrin gene (FLG) mutations and disease severity.


METHODS
Adult patients with AD (n = 101) were included in the study. Bacterial swabs were taken from lesional skin, nonlesional skin and the nose. Swabs positive for S. aureus were characterized by spa and the respective clonal complex (CC) type assigned. Patients were characterized with respect to disease severity (Scoring Atopic Dermatitis) and FLG mutations (n = 88). Fisher's exact test was used to analyse differences in S. aureus colonization in relation to FLG mutations.


RESULTS
Of the 101 patients included, 74 (73%) were colonized with S. aureus. Of the colonized patients, 70 (95%) carried only one CC type in all three different sampling sites. In lesional skin, S. aureus was found in 24 of 31 patients with FLG mutations vs. 24 of 54 wild-type patients (P = 0·0004). Staphylococcus aureusCC1 clonal lineage was more prevalent in patients with FLG mutations (n = 10) than in wild-type patients (n = 2) (P = 0·003). No specific bacterial lineage was linked to disease severity.


CONCLUSIONS
Increased S. aureus colonization in patients with AD with FLG mutations, and increased prevalence of CC1 in patients with FLG mutations, suggest that host-microbe interactions and clonal differences in S. aureus are important for colonization of AD skin.
Department of Dermatology, Bispebjerg University Hospital, Copenhagen, Denmark.
M-L
http://orcid.org/0000-0003-4517-5376
ML
Clausen
Department of Microbiology and Infection Control, Statens Serum Institut, Copenhagen, Denmark.
S M
SM
Edslev
Department of Microbiology and Infection Control, Statens Serum Institut, Copenhagen, Denmark.|Institute of Veterinary Disease Biology, University of Copenhagen, Copenhagen, Denmark.
P S
PS
Andersen
Department of Dermatology, Bispebjerg University Hospital, Copenhagen, Denmark.
K
K
Clemmensen
Department of Microbiology and Infection Control, Statens Serum Institut, Copenhagen, Denmark.
K A
KA
Krogfelt
Department of Dermatology, Bispebjerg University Hospital, Copenhagen, Denmark.
T
T
Agner
D000328:Adult; D000368:Aged; D001426:Bacterial Proteins / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000235:genetics / Q000382:microbiology*; D005260:Female; D000091344:Filaggrin Proteins; D054884:Host-Pathogen Interactions / Q000235:genetics*; D006801:Humans; D007381:Intermediate Filament Proteins / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics*; D009668:Nose Diseases / Q000235:genetics / Q000382:microbiology*; D013203:Staphylococcal Infections / Q000235:genetics*; D013207:Staphylococcal Skin Infections / Q000235:genetics; D013211:Staphylococcus aureus / Q000145:classification; D055815:Young Adult
D001426:Bacterial Proteins; C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D007381:Intermediate Filament Proteins