Neutrophil activation in nickel sensitized subjects.
Conflicting results were obtained from the evaluation of nickel-mediated effects on immunoresponsiveness. A reduction of B cell polyclonal response, mixed lymphocyte reaction, T lymphocyte proliferation and natural killer cytotoxicity was evident following nickel salt exposure. On the contrary, an enhancement of cytokine release, T cell proliferative capacity and adhesion molecule expression was found in nickel sensitized donors. In addition, under different experimental conditions, respiratory burst induction and myeloperoxidase release by polymorphonuclear cells (PMN) in a group of individuals exhibiting nickel hypersensitivity were investigated. Results provide evidence that nickel allergic individuals displayed a significant increase of superoxide anion (O2-) generation by suspended PMN in comparison with similar cell suspensions from healthy donors, but this was not the case when adherent neutrophils were used as effector cells. PMN from nickel sensitized donors exhibited a significant enhancement of hydrogen peroxide (H2O2) and myeloperoxidase release. The results imply the occurrence of neutrophil activation in nickel hypersensitivity, which in turn may be responsible for the low frequency of life-threatening infections in these subjects.
Testa
A
A
Department of Internal Medicine, University of Bari Medical School, Italy.
Serrone
M
M
Foti
C
C
Assennato
G
G
Jirillo
E
E
Antonaci
S
S
D000328:Adult; D004198:Disease Susceptibility; D004342:Drug Hypersensitivity / Q000209:etiology / Q000276:immunology*; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D007239:Infections / Q000276:immunology; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism; D009532:Nickel / Q000009:adverse effects*; D009195:Peroxidase / Q000378:metabolism; D016897:Respiratory Burst
D009532:Nickel; D006861:Hydrogen Peroxide; D009195:Peroxidase