Michelangelo Di Giuseppe

TL;DR: It is shown that MSCs manage intracellular oxidative stress by targeting depolarized mitochondria to the plasma membrane via arrestin domain-containing protein 1-mediated microvesicles and simultaneously shed micro RNA-containing exosomes that inhibit macrophage activation by suppressing Toll-like receptor signalling.

TL;DR: Evaluated lung transplant database data support that patients with silicosis appear to have poor outcome following lung transplantation, and experimental data indicate that while the systemic inhibition of NF-κB protects from silica-induced lung injury, epithelial cell specific NF-σκB inhibition appears to aggravate the outcome of experimentalsilicosis.

TL;DR: Novel data is presented showing that crystalline silica particles with a geometric mean of 0.3 μm enhance the activation of AM when compared to largersilica particles usually represented in in vitro and in vivo research.

TL;DR: It is demonstrated that reduced p47phox expression in IC21 macrophages is linked to enhanced mtROS generation, cardiolipin oxidation, and accumulation of cardiolaipin hydrolysis products, culminating in cell death.

TL;DR: It is suggested that macrophages participate in the repression of SFTPB expression by LPS, and that Macrophage-released cytokines (including TNF) regulate the transcription factor CEBPB, which can function as a downstream transcriptional repressor ofSFTPB gene expression in pulmonary epithelial cells.