title: Oral antibiotic treatment induces skin microbiota dysbiosis and influences wound healing.
abstract: Antibiotic treatment eliminates commensal bacteria and impairs mucosal innate immune defenses in the gut. However, whether oral antibiotic treatment could alter the composition of the microbiota on the skin surface and influence innate immune responses remains unclear. To test this, mice were treated with vancomycin for 7 days and then wounds were made on the back skin of the mice. Five days later, scar tissue from each mouse was collected for bacterial enumeration, the bacterial composition on the scar and unwounded skin was determined using 16S RNA gene-based pyrosequencing analysis, and skin around wounds was collected for RNA extraction. Compared with the control group, the overall density and composition of skin bacteria were altered, and the proportion of Staphylococcus-related sequences was reduced in the vancomycin-treated group. Moreover, vancomycin treatment decreased the expression of RegIIIγ and interleukin (IL)-17 in the wounded skin. Taken together, our data demonstrate that antibiotic treatment decreases the bacterial density and alters the bacterial composition in skin wounds, followed by a decrease in RegIIIγ expression, which may contribute to the delayed wound repair. Our findings also indicate that antibiotic therapy should be carefully considered in the treatment of skin injury.
authors.affiliation: Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, No. 500 Minhang Dongchuan Road, Shanghai, 200241, People's Republic of China.
authors.forename: Meiling
authors.initials: M
authors.lastname: Zhang
authors.forename: Ziwei
authors.initials: Z
authors.lastname: Jiang
authors.forename: Dongqing
authors.initials: D
authors.lastname: Li
authors.forename: Deming
authors.initials: D
authors.lastname: Jiang
authors.forename: Yelin
authors.initials: Y
authors.lastname: Wu
authors.forename: Hongyan
authors.initials: H
authors.lastname: Ren
authors.forename: Hua
authors.initials: H
authors.lastname: Peng
authors.forename: Yuping
authors.initials: Y
authors.lastname: Lai
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000900:Anti-Bacterial Agents / Q000009:adverse effects*; D058491:Bacterial Load; D019295:Computational Biology; D015536:Down-Regulation; D064806:Dysbiosis / Q000139:chemically induced / Q000382:microbiology*; D020381:Interleukin-17 / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D064307:Microbiota; D000073718:Pancreatitis-Associated Proteins; D011506:Proteins / Q000235:genetics / Q000378:metabolism; D012329:RNA, Bacterial / Q000235:genetics; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D012867:Skin / Q000187:drug effects* / Q000382:microbiology; D013210:Staphylococcus / Q000187:drug effects; D014640:Vancomycin / Q000009:adverse effects; D014945:Wound Healing / Q000187:drug effects*
chemical_list: D000900:Anti-Bacterial Agents; D020381:Interleukin-17; D000073718:Pancreatitis-Associated Proteins; D011506:Proteins; D012329:RNA, Bacterial; D012336:RNA, Ribosomal, 16S; C490255:Reg3g protein, mouse; D014640:Vancomycin