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一甲基胂酸(MMAIII)对人支气管上皮细胞对铜绿假单胞菌的固有免疫反应有不利影响。

Monomethylarsonous Acid (MMAIII) Has an Adverse Effect on the Innate Immune Response of Human Bronchial Epithelial Cells to Pseudomonas aeruginosa.

作者信息

Notch Emily G, Goodale Britton C, Barnaby Roxanna, Coutermarsh Bonita, Berwin Brent, Taylor Vivien F, Jackson Brian P, Stanton Bruce A

机构信息

Department of Microbiology and Immunology, Center for Environmental Health Sciences, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.

Department of Physical and Biological Sciences, Western New England University, Springfield, Massachusetts, United States of America.

出版信息

PLoS One. 2015 Nov 10;10(11):e0142392. doi: 10.1371/journal.pone.0142392. eCollection 2015.

Abstract

UNLABELLED

Arsenic is the number one contaminant of concern with regard to human health according to the World Health Organization. Epidemiological studies on Asian and South American populations have linked arsenic exposure with an increased incidence of lung disease, including pneumonia, and chronic obstructive pulmonary disease, both of which are associated with bacterial infection. However, little is known about the effects of low dose arsenic exposure, or the contributions of organic arsenic to the innate immune response to bacterial infection. This study examined the effects on Pseudomonas aeruginosa (P. aeruginosa) induced cytokine secretion by human bronchial epithelial cells (HBEC) by inorganic sodium arsenite (iAsIII) and two major metabolites, monomethylarsonous acid (MMAIII) and dimethylarsenic acid (DMAV), at concentrations relevant to the U.S.

POPULATION

Neither iAsIII nor DMAV altered P. aeruginosa induced cytokine secretion. By contrast, MMAIII increased P. aeruginosa induced secretion of IL-8, IL-6 and CXCL2. A combination of iAsIII, MMAIII and DMAV (10 pbb total) reduced IL-8 and CXCL1 secretion. These data demonstrate for the first time that exposure to MMAIII alone, and a combination of iAsIII, MMAIII and DMAV at levels relevant to the U.S. may have negative effects on the innate immune response of human bronchial epithelial cells to P. aeruginosa.

摘要

未标记

根据世界卫生组织的说法,砷是与人类健康相关的首要污染物。对亚洲和南美人群的流行病学研究表明,砷暴露与肺部疾病发病率增加有关,包括肺炎和慢性阻塞性肺疾病,这两种疾病都与细菌感染有关。然而,关于低剂量砷暴露的影响,或有机砷对细菌感染先天免疫反应的贡献,人们知之甚少。本研究检测了与美国相关浓度下,无机亚砷酸钠(iAsIII)及其两种主要代谢产物一甲基亚砷酸(MMAIII)和二甲基砷酸(DMAV)对人支气管上皮细胞(HBEC)分泌铜绿假单胞菌(P. aeruginosa)诱导的细胞因子的影响。

人群

iAsIII和DMAV均未改变铜绿假单胞菌诱导的细胞因子分泌。相比之下,MMAIII增加了铜绿假单胞菌诱导的IL-8、IL-6和CXCL2分泌。iAsIII、MMAIII和DMAV的组合(总量为10 pbb)减少了IL-8和CXCL1分泌。这些数据首次表明,单独暴露于MMAIII以及与美国相关水平的iAsIII、MMAIII和DMAV组合,可能会对人支气管上皮细胞对铜绿假单胞菌的先天免疫反应产生负面影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/110e/4640536/8e9674319bf3/pone.0142392.g001.jpg

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