title: Longitudinal shift in diabetic wound microbiota correlates with prolonged skin defense response.
abstract: Diabetics frequently suffer from chronic, nonhealing wounds. Although bacterial colonization and/or infection are generally acknowledged to negatively impact wound healing, the precise relationship between the microbial community and impaired wound healing remains unclear. Because the host cutaneous defense response is proposed to play a key role in modulating microbial colonization, we longitudinally examined the diabetic wound microbiome in tandem with host tissue gene expression. By sequencing 16S ribosomal RNA genes, we show that a longitudinal selective shift in wound microbiota coincides with impaired healing in diabetic mice (Lepr(db/db); db/db). We demonstrate a parallel shift in longitudinal gene expression that occurs in a cluster of genes related to the immune response. Further, we establish a correlation between relative abundance of Staphylococcus spp. and the expression of cutaneous defense response genes. Our data demonstrate that integrating two types of global datasets lends a better understanding to the dynamics governing host-microbe interactions.
authors.affiliation: Genetics and Molecular Biology Branch, National Institutes of Health Intramural Sequencing Center, National Human Geome Research Institute, Bethesda, MD 20892, USA.
authors.forename: Elizabeth A
authors.initials: EA
authors.lastname: Grice
authors.forename: Evan S
authors.initials: ES
authors.lastname: Snitkin
authors.forename: Laura J
authors.initials: LJ
authors.lastname: Yockey
authors.forename: Dustin M
authors.initials: DM
authors.lastname: Bermudez
authors.forename: Kenneth W
authors.initials: KW
authors.lastname: Liechty
authors.forename: Julia A
authors.initials: JA
authors.lastname: Segre
mesh_terms: D000818:Animals; D001419:Bacteria / Q000145:classification / Q000235:genetics / Q000254:growth & development; D001424:Bacterial Infections / Q000235:genetics / Q000382:microbiology / Q000503:physiopathology*; D044822:Biodiversity; D016000:Cluster Analysis; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000503:physiopathology*; D005260:Female; D020869:Gene Expression Profiling; D054884:Host-Pathogen Interactions; D054892:Metagenome / Q000235:genetics; D051379:Mice; D018345:Mice, Knockout; D008969:Molecular Sequence Data; D011157:Population Dynamics; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D054411:Receptors, Leptin / Q000235:genetics / Q000502:physiology; D017422:Sequence Analysis, DNA; D012867:Skin / Q000378:metabolism / Q000382:microbiology / Q000503:physiopathology*; D013210:Staphylococcus / Q000235:genetics / Q000502:physiology; D013997:Time Factors; D014945:Wound Healing
chemical_list: D012336:RNA, Ribosomal, 16S; D054411:Receptors, Leptin; C515447:leptin receptor, mouse