Chronic Arsenic Exposure Impairs Macrophage Functions in the Exposed Individuals

被引:70
作者
Banerjee, Nilanjana [1 ]
Banerjee, Saptarshi [2 ]
Sen, Rupashree [3 ]
Bandyopadhyay, Apurba [1 ]
Sarma, Nilendu [4 ]
Majumder, Papiya [5 ]
Das, Jayanta K. [6 ]
Chatterjee, Mitali [3 ]
Kabir, Syed N. [7 ]
Giri, Ashok K. [1 ]
机构
[1] Indian Inst Chem Biol, Mol & Human Genet Div, Kolkata 700032, India
[2] Ramkrishna Mission Seva Pratisthan, Dept Ophthalmol, Kolkata, India
[3] Inst Post Grad Med Educ & Res, Dept Pharmacol, Kolkata 700020, India
[4] Sir Nil Ratan Sircar Med Coll & Hosp, Kolkata, India
[5] Peerless Hosp & BC Roy Res Ctr, Kolkata, India
[6] W Bank Hosp, Dept Dermatol, Howrah 711109, India
[7] Indian Inst Chem Biol, Cell Biol & Physiol Div, Kolkata 700032, India
关键词
Arsenic; cell adhesion; macrophage; phagocytosis; Rho A-ROCK pathway; WEST-BENGAL; DRINKING-WATER; CYTOKINE SECRETION; INORGANIC ARSENITE; GENE-EXPRESSION; GROWTH-FACTOR; SKIN-LESIONS; CELLS; DIFFERENTIATION; APOPTOSIS;
D O I
10.1007/s10875-009-9304-x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Owing to the established roles of human macrophages in immune defense, we investigated the effect of chronic arsenic exposure upon these major hematopoietic cells in 70 arsenic-exposed individuals with skin lesions and 64 unexposed individuals. Human monocyte-derived macrophages were prepared from peripheral blood mononuclear cells, by culture of the adherent cells for 6 days in medium supplemented with granulocyte-monocyte colony stimulating factor. Parameters studied included cell adhesion capacity, expression of CD54 and F-actin, nitric oxide production, phagocytic capacity, and effect of arsenic on Rho A-ROCK pathway. In macrophages of exposed individuals when compared to unexposed group, there was cell rounding accompanied with a significant (p < 0.001) loss of cell adhesion capacity, decrease in nitric oxide production, impaired phagocytic capacity, and decreased CD 54 and F-actin expression. Additionally, chronic arsenic exposure affected Rho A-ROCK pathway which in turn impaired macrophage functions. These altogether could contribute significantly to arsenic-induced immunosuppression observed in the arsenic-exposed individuals.
引用
收藏
页码:582 / 594
页数:13
相关论文
共 46 条
[1]   Functional heterogeneity of colony-stimulating factor-induced human monocyte-derived macrophages [J].
Akagawa, KS .
INTERNATIONAL JOURNAL OF HEMATOLOGY, 2002, 76 (01) :27-34
[2]  
Allen WE, 1997, J CELL SCI, V110, P707
[3]   Cancer incidence after immunosuppressive treatment following kidney transplantation [J].
Andrés, A .
CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY, 2005, 56 (01) :71-85
[4]   Genomic and proteomic profiling of responses to toxic metals in human lung cells [J].
Andrew, AS ;
Warren, AJ ;
Barchowsky, A ;
Temple, KA ;
Klei, L ;
Soucy, NV ;
O'Hara, KA ;
Hamilton, JW .
ENVIRONMENTAL HEALTH PERSPECTIVES, 2003, 111 (06) :825-838
[5]  
[Anonymous], 1999, Arsenic in drinking water
[6]  
[Anonymous], 1996, Guidelines for drinking-water quality, V2, P940
[7]  
ATSDR, 1999, TOX PROF ARS
[8]   Polymorphism in the ERCC2 codon 751 is associated with arsenic-induced premalignant hyperkeratosis and significant chromosome aberrations [J].
Banerjee, Mayukh ;
Sarkar, Jyotirmoy ;
Das, Jayanta K. ;
Mukherjee, Angshuman ;
Sarkar, Ajoy K. ;
Mondal, Lakshmikanta ;
Giri, Ashok K. .
CARCINOGENESIS, 2007, 28 (03) :672-676
[9]   Arsenic-induced mitochondrial instability leading to programmed cell death in the exposed individuals [J].
Banerjee, Nilanjana ;
Banerjee, Mayukh ;
Ganguly, Sudipto ;
Bandyopadhyay, Santu ;
Das, Jayanta K. ;
Bandyopadhay, Apurba ;
Chatterjee, Mitali ;
Giri, Ashok K. .
TOXICOLOGY, 2008, 246 (2-3) :101-111
[10]  
Basu A, 2004, CANCER EPIDEM BIOMAR, V13, P820