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Chronic Low-Dose Cadmium Exposure Impairs Cutaneous Wound Healing With Defective Early Inflammatory Responses After Skin Injury

文献类型：期刊论文

作者Mei, Hong4,5; Yao, Pengle4,5; Wang, Shanshan4,5; Li, Na4,5; Zhu, Tengfei4,5; Chen, Xiaofang4,5; Yang, Mengmei4,5; Zhuo, Shu4,5; Chen, Shiting4,5; Wang, Hui4,5
刊名TOXICOLOGICAL SCIENCES
出版日期2017
卷号159期号:2页码:327-338
关键词cadmium wound healing neutrophil chemokine proinflammatory cytokine
ISSN号1096-6080
DOI10.1093/toxsci/kfx137
文献子类Article
英文摘要Impairment of the immune system is a developing concern in evaluating the toxicity of cadmium (Cd). In the present study, we investigated if Cd could impair cutaneous wound healing through interfering with inflammation after injury. We found that exposure of mice to CdCl2 through drinking water at doses of 10, 30, and 50 mg/l for 8 weeks significantly impaired cutaneous wound healing. Chronic 30 mg/l CdCl2 treatment elevated murine blood Cd level comparable to that of low dose Cd-exposed humans, had no effect on blood total and differential leukocyte counts, but reduced neutrophil infiltration, chemokines (CXCL1 and CXCL2), and proinflammatory cytokines (TNF alpha, IL-1 beta, and IL-6) expression in wounded tissue at early stage after injury. Wounded tissue homogenates from CdCl2-treated mice had lower chemotactic activity for neutrophils than those from untreated mice. Mechanistic studies showed that chronic Cd treatment suppressed ERK1/2 and NF-kappa B p65 phosphorylation in wounded tissue at early stage after injury. Compared with neutrophils isolated from untreated mice, neutrophils from CdCl2 treated mice and normal neutrophils treated with CdCl2 invitro both had lower chemotactic response, calcium mobilization and ERK1/2 phosphorylation upon chemoattractant stimulation. Collectively, our study indicate that chronic low-dose Cd exposure impaired cutaneous wound healing by reducing neutrophil infiltration through inhibiting chemokine expression and neutrophil chemotactic response, and suppressing proinflammatory cytokine expression. Cd may suppress chemokine and proinflammatory expression through inactivating ERK1/2 and NF-kappa B, and inhibit neutrophil chemotaxis by attenuating calcium mobilization and ERK1/2 phosphorylation in response to chemoattractants.
学科主题Toxicology
WOS关键词OPERATED CALCIUM-ENTRY ; INDUCED APOPTOSIS ; HUMAN NEUTROPHILS ; ACTIVATION ; MICE ; CELLS ; RECEPTORS ; CYTOKINES ; PATHWAYS ; BLOOD
语种英语
WOS记录号WOS:000412203900004
出版者OXFORD UNIV PRESS
版本出版稿
源URL[http://202.127.25.144/handle/331004/793]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA;
2.Minist Hlth, Key Lab food safety risk Assessment, Beijing 100021, Peoples R China;
3.Soochow Univ, Ruihua Affiliated Hosp, Inst Hand Surg, Suzhou 215104, Peoples R China,
4.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab food safety Res, 320 Yueyang Rd, Shanghai 200031, Peoples R China;
5.Univ Chinese Acad Sci, Shanghai 200031, Peoples R China;
推荐引用方式
GB/T 7714		 Mei, Hong,Yao, Pengle,Wang, Shanshan,et al. Chronic Low-Dose Cadmium Exposure Impairs Cutaneous Wound Healing With Defective Early Inflammatory Responses After Skin Injury[J]. TOXICOLOGICAL SCIENCES,2017,159(2):327-338.
APA Mei, Hong.,Yao, Pengle.,Wang, Shanshan.,Li, Na.,Zhu, Tengfei.,...&,.(2017).Chronic Low-Dose Cadmium Exposure Impairs Cutaneous Wound Healing With Defective Early Inflammatory Responses After Skin Injury.TOXICOLOGICAL SCIENCES,159(2),327-338.
MLA Mei, Hong,et al."Chronic Low-Dose Cadmium Exposure Impairs Cutaneous Wound Healing With Defective Early Inflammatory Responses After Skin Injury".TOXICOLOGICAL SCIENCES 159.2(2017):327-338.

入库方式： OAI收割

来源：上海营养与健康研究所

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