title: Lidocaine inhibits staphylococcal enterotoxin-stimulated activation of peripheral blood mononuclear cells from patients with atopic dermatitis.
abstract: Atopic dermatitis (AD) is an inflammatory, chronically relapsing, pruritic skin disease and lesions associated with AD are frequently colonized with Staphylococcus aureus (S. aureus). Activation of T cells by staphylococcal enterotoxins (SE) plays a crucial role in the pathogenesis of AD. Previous studies have demonstrated that lidocaine could attenuate allergen-induced T cell proliferation and cytokine production in peripheral blood mononuclear cells (PBMCs) from asthma patients. The purpose of this study was to investigate the effects of lidocaine on SE-stimulated activation of PBMCs from AD patients. PBMCs were isolated from ten AD patients and stimulated by staphylococcal enterotoxin A (SEA) or staphylococcal enterotoxin B (SEB) in the presence or absence of lidocaine in various concentrations. Cellular proliferation and the release of representative TH1- and TH2-type cytokines were measured. The effect of lidocaine on filaggrin (FLG) expression in HaCaT cells co-cultured with SE-activated PBMCs was also examined. Our results demonstrated that lidocaine dose-dependently inhibited the proliferative response and the release of IL-4, IL-5, IL-13, TNF-α, and IFN-γ from SEA- and SEB-stimulated PBMCs and also blocked the down-regulation of FLG expression in HaCaT cells co-cultured with SEA- and SEB-activated PBMCs. These results indicate that lidocaine inhibited SEA- and SEB-stimulated activation of PBMCs from patients with AD. Our findings encourage the use of lidocaine in the treatment of AD.
authors.affiliation: Department of Dermatology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, China.
authors.forename: Qingqing
authors.initials: Q
authors.lastname: Jiao
authors.forename: Honglin
authors.initials: H
authors.lastname: Wang
authors.forename: Zhenglin
authors.initials: Z
authors.lastname: Hu
authors.forename: Yin
authors.initials: Y
authors.lastname: Zhuang
authors.forename: Weiqin
authors.initials: W
authors.lastname: Yang
authors.forename: Ming
authors.initials: M
authors.lastname: Li
authors.forename: Xia
authors.initials: X
authors.lastname: Yu
authors.forename: Jianying
authors.initials: J
authors.lastname: Liang
authors.forename: Yifeng
authors.initials: Y
authors.lastname: Guo
authors.forename: Hui
authors.initials: H
authors.lastname: Zhang
authors.forename: Xilan
authors.initials: X
authors.lastname: Chen
authors.forename: Ruhong
authors.initials: R
authors.lastname: Cheng
authors.forename: Zhirong
authors.initials: Z
authors.lastname: Yao
mesh_terms: D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D018920:Coculture Techniques; D016207:Cytokines / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000473:pathology; D015536:Down-Regulation / Q000187:drug effects; D004768:Enterotoxins / Q000276:immunology; D005260:Female; D000091344:Filaggrin Proteins; D006801:Humans; D007381:Intermediate Filament Proteins / Q000235:genetics / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects; D008012:Lidocaine / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects; D008297:Male; D013211:Staphylococcus aureus / Q000378:metabolism*; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology*; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology*
chemical_list: D016207:Cytokines; D004768:Enterotoxins; C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D007381:Intermediate Filament Proteins; C026066:enterotoxin A, Staphylococcal; C031818:enterotoxin B, staphylococcal; D008012:Lidocaine