Bisphenol A, bisphenol S and their glucuronidated metabolites modulate glycolysis and functional responses of human neutrophils

Bisphenol A (BPA) and its main substitute, bisphenol S (BPS), are synthetic organic compounds found in various consumer products, in particular food and beverage containers. Numerous reports have shown a link between bisphenol exposure, human contamination and increased health problems. BPA, BPS and their metabolites are detectable in bodily fluids (blood, urine) and were reported to affect immune cells and their responses. Though, the impact of those chemicals on neutrophils, the most abundant leukocytes in the circulation, remains poorly described. Therefore, we examined the effects of BPA, BPS and their monoglucuronide conjugates on neutrophil energy metabolism and anti-microbial functions, mainly phagocytosis, superoxide anion generation and CXCL8/IL-8 chemokine production. We observed that short and prolonged exposures of neutrophils to these chemicals modulate the basal and the bacterium-derived peptide N-formyl-methionyl-leucyl-phenylalanine-induced glycolysis, with BPS causing the most alterations. The variation in energy metabolism was not associated with dysfunctions in cell cytotoxicity, phagocytosis, nor superoxide anion production upon exposure to bisphenols. In contrast, bisphenols significantly reduced the production of CXCL8/IL-8 by neutrophils, an effect found to be greater with the glucuronidated metabolites. Our study highlights that BPA, BPS and their glucuronidated metabolites alter the energy metabolism and certain anti-microbial responses of neutrophils, with possible health implications. Importantly, we found that BPS and the glucuronidated metabolites of BPA and BPS showed higher endocrine-disrupting potential than BPA. More studies on bisphenols, especially the less-documented BPS and bisphenol metabolites, are needed to fully determine their risks, allow better regulation of these compounds, and restrict their extensive usage

Study of electrical properties of Al/Si 3 N 4 / n -GaAs MIS capacitors deposited at low and high frequency PECVD

International audienceAs for silicon, surface passivation of GaAs and III-V semiconductors using silicon nitride (Si 3 N 4 ) deposited by plasma enhanced chemical deposition (PECVD) is widely used to improve devices and circuits stability, reliability and for encapsulation. In this work, the effect of plasma excitation frequency in the PECVD reactor on the surface passivation efficiency of GaAs during Si 3 N 4 deposition was investigated. Metal-Insulator-Semiconductor (Al/Si 3 N 4 / n -GaAs) capacitors are fabricated and characterized using capacitance–voltage ( C – V ), and conductance–voltage ( G – V ) to compare electronic properties of GaAs/Si 3 N 4 interfaces depending on the use of a high frequency PECVD (HF-PECVD) or low frequency (LF-PECVD) process. The drastic advantage of using the LF-PECVD technique for the passivation of GaAs is clearly demonstrated on the characteristic C – V at 1 MHz where a good surface potential was observed, while a quasi-pinned surface Fermi level was found when HF-PECVD was used. To unpin Fermi level, a sulfur pre-treatment prior before HF-PECVD deposition and post-metallisation annealing were necessary. A lower frequency dispersion and a lower hysteresis indicating low densities of slow traps were observed for MIS devices fabricated by LF-PECVD. The advantage of having an efficient passivation without sulfur treatment is important since ammonium sulfide used for this purpose is corrosive and difficult to adapt in industrial environment. The better electronic properties of GaAs/Si 3 N 4 interface were found for silicon nitride layers using LF-PECVD deposition. This can probably be associated with the high-level injection of H + ions on the semiconductor surface reducing thus the native oxides during the initial steps of dielectric deposition

Enhanced myelopoiesis and aggravated arthritis in S100a8-deficient mice.

Expressed strongly by myeloid cells, damage-associated molecular pattern (DAMP) proteins S100A8 and S100A9 are found in the serum of patients with infectious and autoimmune diseases. Compared to S100A9, the role of S100A8 is controversial. We investigated its biological activity in collagen-induced arthritis using the first known viable and fertile S100a8-deficient (S100a8-/-) mouse. Although comparable to the wild type (WT) in terms of lymphocyte distribution in blood and in the primary and secondary lymphoid organs, S100a8-/- mice had increased numbers of neutrophils, monocytes and dendritic cells in the blood and bone marrow, and these all expressed myeloid markers such as CD11b, Ly6G and CD86 more strongly. Granulocyte-macrophage common precursors were increased in S100a8-/- bone marrow and yielded greater numbers of macrophages and dendritic cells in culture. The animals also developed more severe arthritic disease leading to aggravated osteoclast activity and bone destruction. These findings were correlated with increased inflammatory cell infiltration and cytokine secretion in the paws. This study suggests that S100A8 is an anti-inflammatory DAMP that regulates myeloid cell differentiation, thereby mitigating the development of experimental arthritis