title: IL-33 promotes Staphylococcus aureus-infected wound healing in mice.
abstract: Interleukin (IL)-33, a newly identified member of IL-1 family of cytokines, plays a crucial role in polarizing Th2-associated immune responses. Recently growing evidence indicates that IL-33 also represents an important mediator of mucosal healing and epithelial restoration. In this study, we investigated the effect of IL-33 on antimicrobial infection and wound healing using a Staphylococcus aureus-infected incision model in mice. Our findings showed that the expression of IL-33 mRNA and protein was promptly increased in cutaneous wound tissues when challenged by methicillin-resistant S. aureus (MRSA). At the same time, exogenous IL-33 administration profoundly inhibited MRSA colonization and accelerated cutaneous wound repair. IL-33 upregulation promoted the proliferation of neutrophils and CXCR2 expression, which is related to augmented neutrophil trafficking into infectious sites for bactericidal effect. In addition, the beneficial effect of IL-33 is also implicated in enhancement of collagen deposition and the expression of extracellular matrix (ECM)-associated genes such as fibronectin and collagen IIIa, which implies a potential effect of IL-33 on matrix synthesis and reepithelialization during the wound repair process. All together, these findings reveal that IL-33 plays an essential effect in maintenance of cutaneous homeostasis and improvement of infectious wound healing.
authors.affiliation: Department of Microbiology and Immunology, Guangdong Pharmaceutical University, Guangzhou, China. huiyin0103@163.com
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: Qian
authors.initials: Q
authors.lastname: Ni
authors.forename: Fang
authors.initials: F
authors.lastname: Lan
authors.forename: Xiaochun
authors.initials: X
authors.lastname: Luo
authors.forename: Hongbiao
authors.initials: H
authors.lastname: Gu
authors.forename: Fang
authors.initials: F
authors.lastname: Zheng
mesh_terms: D000818:Animals; D058491:Bacterial Load / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D024061:Collagen Type III / Q000378:metabolism; D005109:Extracellular Matrix / Q000187:drug effects; D005353:Fibronectins / Q000378:metabolism; D000067596:Interleukin-33; D007378:Interleukins / Q000008:administration & dosage / Q000235:genetics / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009504:Neutrophils / Q000276:immunology*; D023063:Receptors, Interleukin-8B / Q000378:metabolism; D012867:Skin / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D013203:Staphylococcal Infections / Q000276:immunology* / Q000628:therapy*; D013211:Staphylococcus aureus / Q000276:immunology*; D014945:Wound Healing / Q000187:drug effects / Q000276:immunology
chemical_list: D024061:Collagen Type III; D005353:Fibronectins; C506535:Il33 protein, mouse; D000067596:Interleukin-33; D007378:Interleukins; D023063:Receptors, Interleukin-8B
keywords: Bacteria; IL-33; Infection; Neutrophil; Wound healing