Temporal and Spatial Variation of the Skin-Associated Bacteria from Healthy Participants and Atopic Dermatitis Patients

被引:6
作者
Barnes, Christopher J. [1 ]
Clausen, Maja-Lisa [2 ]
Asplund, Maria [1 ]
Rasmussen, Linett [1 ]
Olesen, Caroline Meyer [2 ]
Yusel, Yasemin Topal [2 ]
Andersen, Paal Skytt [3 ]
Litman, Thomas [4 ]
Hansen, Anders Johannes [1 ]
Agner, Tove [2 ]
机构
[1] Univ Copenhagen, Fac Hlth, Globe Inst, Copenhagen, Denmark
[2] Univ Copenhagen, Bispebjerg Hosp, Dept Dermatol, Copenhagen, Denmark
[3] Statens Serum Insitute, Dept Bacteria Parasites & Fungi, Copenhagen, Denmark
[4] Univ Copenhagen, LEO Fdn Skin Immunol Res Ctr, Dept Immunol & Microbiol, Copenhagen, Denmark
关键词
Atopic dermatitis; eczema; metabarcoding; Staphylococcus aureus; skin microbiome; spatial-temporal variation; bacteria; atopic dermatitis; temporal variation; MICROBIOME; DIVERSITY; COMMUNITIES; ECZEMA; DADA2;
D O I
10.1128/msphere.00917-21
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Several factors have been shown to influence the composition of the bacterial communities inhabiting healthy skin, with variation between different individuals, differing skin depths, and body locations (spatial-temporal variation). Atopic dermatitis (AD) is a chronic skin disease also affecting the skin-associated bacterial communities. While the effects of AD have been studied on these processes individually, few have considered how AD disrupts the spatial-temporal variation of the skin bacteria as a whole (i.e., considered these processes simultaneously). Here, we characterized the skin-associated bacterial communities of healthy volunteers and lesional and nonlesional skin of AD patients by metabarcoding the universal V3-V4 16S rRNA region from tape strip skin samples. We quantified the spatial-temporal variation (interindividual variation, differing skin depths, multiple time points) of the skin-associated bacteria within healthy controls and AD patients, including the relative change induced by AD in each. Interindividual variation correlated with the bacterial community far more strongly than any other factors followed by skin depth and then AD status. There was no significant temporal variation found within either AD patients or healthy controls. The bacterial community was found to vary markedly according to AD severity, and between patients without and with filaggrin mutations. Therefore, future studies may benefit from sampling subsurface epidermal communities and considering AD severity and the host genome in understanding the role of the skin bacterial community within AD pathogenesis rather than considering AD as a presence-absence disorder. IMPORTANCE The bacteria associated with human skin may influence skin barrier function and the immune response. Previous studies have attempted to understand the factors that regulate the skin bacteria, characterizing the spatial-temporal variation of the skin bacteria within unaffected skin. Here, we quantified the effect of AD on the skin bacteria on multiple spatial-temporal factors simultaneously. Although significant community variation between healthy controls and AD patients was observed, the effects of AD on the overall bacterial community were relatively low compared to other measured factors. Results here suggest that changes in specific taxa rather than wholesale changes in the skin bacteria are associated with mild to moderate AD. Further studies would benefit from incorporating the complexity of AD into models to better understand the condition, including AD severity and the host genome, alongside microbial composition. The bacteria associated with human skin may influence skin barrier function and the immune response. Previous studies have attempted to understand the factors that regulate the skin bacteria, characterizing the spatial-temporal variation of the skin bacteria within unaffected skin.
引用
收藏
页数:14
相关论文
共 47 条
  • [1] Recent advances in atopic dermatitis
    Ahn, Kangmo
    Kim, Byung Eui
    Kim, Jihyun
    Leung, Donald Y. M.
    [J]. CURRENT OPINION IN IMMUNOLOGY, 2020, 66 : 14 - 21
  • [2] Comparing DADA2 and OTU clustering approaches in studying the bacterial communities of atopic dermatitis
    Barnes, Christopher J.
    Rasmussen, Linett
    Asplund, Maria
    Knudsen, Steen Wilhelm
    Clausen, Maja-Lisa
    Agner, Tove
    Hansen, Anders J.
    [J]. JOURNAL OF MEDICAL MICROBIOLOGY, 2020, 69 (11) : 1293 - 1302
  • [3] Bates D., 2007, The lme4 package. R Package Version, V2, P74
  • [4] Universal Dermal Microbiome in Human Skin
    Bay, Lene
    Barnes, Christopher James
    Fritz, Blaine Gabriel
    Thorsen, Jonathan
    Restrup, Marlene Elise Moller
    Rasmussen, Linett
    Sorensen, Johan Klovgaard
    Hesselvig, Anne Brun
    Odgaard, Anders
    Hansen, Anders Johannes
    Bjarnsholt, Thomas
    [J]. MBIO, 2020, 11 (01):
  • [5] Atopic dermatitis 2.0: from the clinical phenotype to the molecular taxonomy and stratified medicine
    Bieber, Th.
    [J]. ALLERGY, 2012, 67 (12) : 1475 - 1482
  • [6] The human skin microbiome
    Byrd, Allyson L.
    Belkaid, Yasmine
    Segre, Julia A.
    [J]. NATURE REVIEWS MICROBIOLOGY, 2018, 16 (03) : 143 - 155
  • [7] Staphylococcus aureus and Staphylococcus epidermidis strain diversity underlying pediatric atopic dermatitis
    Byrd, Allyson L.
    Deming, Clay
    Cassidy, Sara K. B.
    Harrison, Oliver J.
    Ng, Weng-Ian
    Conlan, Sean
    Belkaid, Yasmine
    Segre, Julia A.
    Kong, Heidi H.
    [J]. SCIENCE TRANSLATIONAL MEDICINE, 2017, 9 (397)
  • [8] Callahan BJ, 2016, NAT METHODS, V13, P581, DOI [10.1038/NMETH.3869, 10.1038/nmeth.3869]
  • [9] Staphylococcus epidermidis protease EcpA can be a deleterious component of the skin microbiome in atopic dermatitis
    Cau, Laura
    Williams, Michael R.
    Butcher, Anna M.
    Nakatsuji, Teruaki
    Kavanaugh, Jeffrey S.
    Cheng, Joyce Y.
    Shafiq, Faiza
    Higbee, Kyle
    Hata, Tissa R.
    Horswill, Alexander R.
    Gallo, Richard L.
    [J]. JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2021, 147 (03) : 955 - 966
  • [10] Chng KR, 2016, NAT MICROBIOL, V1, DOI [10.1038/NMICROBIOL.2016.106, 10.1038/nmicrobiol.2016.106]