8 research outputs found
Genotoxic potential of diesel exhaust particles from the combustion of first- and second-generation biodiesel fuels—the FuelHealth project
Oxidative damage mediates the association between polycyclic aromatic hydrocarbon exposure and lung function
Impacts of particulate matter (PM2.5) on the behavior of freshwater snail Parafossarulus striatulus
Diesel exhaust particle exposure in vitro impacts T lymphocyte phenotype and function
Background: Diesel exhaust particles (DEP) are major constituents of ambient air pollution and their adverse health
effect is an area of intensive investigations. With respect to the immune system, DEP have attracted significant
research attention as a factor that could influence allergic diseases interfering with cytokine production and chemokine
expression. With this exception, scant data are available on the impact of DEP on lymphocyte homeostasis. Here, the
effects of nanoparticles from Euro 4 (E4) and Euro 5 (E5) light duty diesel engines on the phenotype and function of T
lymphocytes from healthy donors were evaluated.
Methods: T lymphocytes were isolated from peripheral blood obtained from healthy volunteers and subsequently
stimulated with different concentration (from 0.15 to 60 μg/ml) and at different time points (from 24 h to 9 days) of
either E4 or E5 particles. Immunological parameters, including apoptosis, autophagy, proliferation levels, mitochondrial
function, expression of activation markers and cytokine production were evaluated by cellular and molecular analyses.
Results: DEP exposure caused a pronounced autophagic-lysosomal blockade, thus interfering with a key mechanism
involved in the maintaining of T cell homeostasis. Moreover, DEP decreased mitochondrial membrane potential but,
unexpectedly, this effect did not result in changes of the apoptosis and/or necrosis levels, as well as of intracellular
content of adenosine triphosphate (ATP). Finally, a down-regulation of the expression of the alpha chain of
the interleukin (IL)-2 receptor (i.e., the CD25 molecule) as well as an abnormal Th1 cytokine expression profile
(i.e., a decrease of IL-2 and interferon (IFN)-γ production) were observed after DEP exposure. No differences
between the two compounds were detected in all studied parameters.
Conclusions: Overall, our data identify functional and phenotypic T lymphocyte parameters as relevant targets
for DEP cytotoxicity, whose impairment could be detrimental, at least in the long run, for human health,
favouring the development or the progression of diseases such as autoimmunity and cancer