Staphylococcus aureus and Staphylococcus epidermidis strain diversity underlying pediatric atopic dermatitis.
Staphylococcus aureus and Staphylococcus epidermidis strain diversity underlying pediatric atopic dermatitis.
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DOI:
10.1126/scitranslmed.aal4651
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发表时间:
2017-07-05
影响因子:
17.1
通讯作者:
Kong HH
中科院分区:
文献类型:
--
作者:
Byrd AL;Deming C;Cassidy SKB;Harrison OJ;Ng WI;Conlan S;NISC Comparative Sequencing Program;Belkaid Y;Segre JA;Kong HH
The heterogeneous course, severity, and treatment responses among patients with atopic dermatitis (AD; eczema) highlight the complexity of this multifactorial disease. Prior studies have used traditional typing methods on cultivated isolates or sequenced a bacterial marker gene to study the skin microbial communities of AD patients. Shotgun metagenomic sequence analysis provides much greater resolution, elucidating multiple levels of microbial community assembly ranging from kingdom to species and strain-level diversification. Here, we analyze microbial temporal dynamics from a cohort of pediatric AD patients sampled throughout the disease course. Species-level investigation of AD flares showed greater Staphylococcus aureus-predominance in patients with more severe disease and S. epidermidis-predominance in patients with less severe disease. At the strain-level, metagenomic sequencing analyses demonstrated clonal S. aureus strains in more severe patients and heterogeneous S. epidermidis strain communities in all patients. To investigate strain-level biological effects of S. aureus, we topically colonized mice with strains isolated from AD patients and controls. This cutaneous colonization model demonstrated S. aureus strain-specific differences in eliciting skin inflammation and immune signatures characteristic of AD patients. Specifically, S. aureus isolates from AD patients with more severe flares induced epidermal thickening and expansion of cutaneous Th2 and Th17 cells. Integrating high-resolution sequencing, culturing, and animal models demonstrated how functional differences of staphylococcal strains may contribute to the complexity of AD disease.
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影响因子:
--
作者:
Galens K;Orvis J;Daugherty S;Creasy HH;Angiuoli S;White O;Wortman J;Mahurkar A;Giglio MG
通讯作者:
Giglio MG
影响因子:
3
作者:
Bardou P;Mariette J;Escudié F;Djemiel C;Klopp C
通讯作者:
Klopp C
影响因子:
3.1
作者:
Kim, Do-Won;Park, Jee-Young;Kim, Jungmin
通讯作者:
Kim, Jungmin
DOI:
10.1073/pnas.1523199113
发表时间:
2016-06-28
影响因子:
11.1
作者:
Bosi, Emanuele;Monk, Jonathan M.;Palsson, Bernhard O.
通讯作者:
Palsson, Bernhard O.
影响因子:
13.8
作者:
Gonzalez ME;Schaffer JV;Orlow SJ;Gao Z;Li H;Alekseyenko AV;Blaser MJ
通讯作者:
Blaser MJ