title: Oleic acid modulation of the immune response in wound healing: a new approach for skin repair.
abstract: Injury triggers inflammatory responses and tissue repair. Several treatments are currently in use to accelerate healing; however, more efficient formulations are still needed for specific injuries. Since unsaturated fatty acids modulate immune responses, we aimed to evaluate their therapeutic effects on wound healing. Skin wounds were induced in BALB/c mice and treated for 5 days with n-3, n-9 fatty acids or vehicle (control). n-9 treated mice presented smaller wounds than control and n-3 at 120 h post-surgery (p.s.). Collagen III mRNA, TIMP1 and MMP9 were significantly elevated in n-9 group compared to n-3 or vehicle at 120 h p.s. Among the inflammatory mediators studied we found that IL-10, TNF-α and IL-17 were also higher in n-9 treated group compared to n-3 or vehicle at 120 h p.s. Interestingly, COX2 had decreased expression on wound tissue treated with n-9. Inflammatory infiltrate analysis revealed diminished frequency of CD4(+), CD8(+) and CD11b(+) cells in n-9 wounds at 24 and 120 h p.s., which was not related to cell death, since in vitro apoptosis experiments did not show any cell damage after fatty acids administration. These results suggested that unsaturated fatty acids, specifically n-9, modulate the inflammation in the wound and enhance reparative response in vivo. n-9 may be a useful tool in the treatment of cutaneous wounds.
authors.affiliation: Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto - USP, Av. Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil.
authors.forename: C R
authors.initials: CR
authors.lastname: Cardoso
authors.forename: S
authors.initials: S
authors.lastname: Favoreto
authors.forename: L L
authors.initials: LL
authors.lastname: Oliveira
authors.forename: J O
authors.initials: JO
authors.lastname: Vancim
authors.forename: G B
authors.initials: GB
authors.lastname: Barban
authors.forename: D B
authors.initials: DB
authors.lastname: Ferraz
authors.forename: J S
authors.initials: JS
authors.lastname: Silva
mesh_terms: D000818:Animals; D017209:Apoptosis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D003094:Collagen / Q000235:genetics; D051546:Cyclooxygenase 2 / Q000235:genetics; D005434:Flow Cytometry; D015870:Gene Expression; D007249:Inflammation; D016753:Interleukin-10 / Q000097:blood; D020381:Interleukin-17 / Q000097:blood; D008042:Linolenic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D008264:Macrophages / Q000276:immunology; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D019301:Oleic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012867:Skin / Q000187:drug effects / Q000254:growth & development / Q000276:immunology* / Q000293:injuries*; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014945:Wound Healing / Q000187:drug effects* / Q000276:immunology*
chemical_list: D020381:Interleukin-17; D008042:Linolenic Acids; D012333:RNA, Messenger; D019715:Tissue Inhibitor of Metalloproteinase-1; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D019301:Oleic Acid; D003094:Collagen; D051546:Cyclooxygenase 2; D020780:Matrix Metalloproteinase 9