title: IL-33 accelerates cutaneous wound healing involved in upregulation of alternatively activated macrophages.
abstract: IL-33 is a recently recognized member of the IL-1 family and has been best identified as a potent inducer of Th2-type immune responses. Increasing evidence, however, indicates that IL-33 also represents an important mediator of mucosal healing and epithelial restoration and repair. In this study, we further explore the potential effect of IL-33 in cutaneous wound healing. A full-thickness skin wound was generated on the back of mice and treated with IL-33 or vehicle intraperitoneally. Our results revealed that the levels of IL-33 mRNA and protein were significantly enhanced in incisional wound skin. Meantime, administration of IL-33 obviously accelerated wound healing with wounds gaping narrower and exhibiting enhanced reepithelialization. IL-33 upregulation also promoted the collagen deposition and the expression of extracellular matrix (ECM)-associated genes such as fibronectin and collagen IIIa, which implies a direct effect of IL-33 on matrix synthesis. Furthermore, IL-33 facilitated the development of alternatively activated macrophages (AAM) in incisional wound tissue, which closely related to resolution of inflammation and promotion of wound repair. Taken together, these findings suggest that IL-33 may play a pivotal role in maintenance of cutaneous homeostasis and acceleration of normal wound healing.
authors.affiliation: Department of Microbiology and Immunology, Guangdong Pharmaceutical University, Guangzhou 510006, China; Guangdong Key Laboratory of Pharmaceutical Bioactive Substances, Guangdong Pharmaceutical University, Guangzhou 510006, China. Electronic address: huiyin0103@yahoo.com.cn.
authors.forename: Hui
authors.initials: H
authors.lastname: Yin
authors.forename: Xiangyong
authors.initials: X
authors.lastname: Li
authors.forename: Shilian
authors.initials: S
authors.lastname: Hu
authors.forename: Tao
authors.initials: T
authors.lastname: Liu
authors.forename: Baohong
authors.initials: B
authors.lastname: Yuan
authors.forename: Hongbiao
authors.initials: H
authors.lastname: Gu
authors.forename: Qian
authors.initials: Q
authors.lastname: Ni
authors.forename: Xiaofan
authors.initials: X
authors.lastname: Zhang
authors.forename: Fang
authors.initials: F
authors.lastname: Zheng
mesh_terms: D000818:Animals; D000943:Antigens, Differentiation / Q000378:metabolism; D003094:Collagen / Q000235:genetics / Q000378:metabolism; D016326:Extracellular Matrix Proteins / Q000235:genetics / Q000378:metabolism; D005353:Fibronectins / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D007150:Immunohistochemistry; D007274:Injections, Intraperitoneal; D000067596:Interleukin-33; D007378:Interleukins / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology*; D037181:Lectins, C-Type / Q000378:metabolism; D008262:Macrophage Activation / Q000187:drug effects*; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D011956:Receptors, Cell Surface / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012867:Skin / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D013997:Time Factors; D015854:Up-Regulation / Q000187:drug effects; D014945:Wound Healing / Q000187:drug effects*
chemical_list: D000943:Antigens, Differentiation; D016326:Extracellular Matrix Proteins; D005353:Fibronectins; C506535:Il33 protein, mouse; D000067596:Interleukin-33; D007378:Interleukins; D037181:Lectins, C-Type; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D011956:Receptors, Cell Surface; C036763:monocyte-macrophage differentiation antigen; D003094:Collagen
keywords: Alternatively activated macrophages; Cytokines; IL-33; Inflammation; Wound healing