Tiziano Verri

Groups of zebrafish (Danio rerio) embryos receive radiations of different frequencies and intensities by means of new prototype devices. They are exposed to static (B0, 0 Hz), extremely low-frequency (ELF, 0.2 Hz), low-frequency (LF, 270 kHz), very-high-frequency (VHF, 100 MHz), and ultra-high-frequency (UHF, 900 MHz) field irradiations. The applied magnetic field intensities are 40 mT at 0 Hz, 40 mT at 0.2 Hz, 470 μT at 270 kHz, 240 nT at 100 MHz, and 240 nT at 900 MHz. Such combinations are meant to cover environmental radiations from geomagnetic fields and cosmic magnetism to electromagnetic radiation of electronic instruments such as GSM and UMTS transmission-mode mobile systems. For each frequency, fish are monitored for up to 5 days. Unexposed embryos are used as controls. Notably, exposure to the different radiations brings alterations of body pigmentation in zebrafish embryos and larvae in terms of total number, area, and morphology of (black) melanophores. This research may contribute to evaluating the roles and effects of magnetic radiation on living matter.

SLC15A4/PHT1 is an endolysosome-resident carrier of oligopeptides and histidine recently come into view as a key path marker of immune/autoimmune/inflammatory pathways in immune cells. Yet, its emerging role in inflammatory processes directly targeting the gastrointestinal epithelial layer, as in the multifactorial pathophysiology of inflammatory bowel disease (IBD), is poorly investigated. Here, the first identification of SLC15A4/PHT1 gene products in human colonic epithelium of ulcerative colitis (UC) patients is reported, showing protein primarily localized in intracellular vesicle-like compartments. Qualitative and quantitative immunohistochemical analyses of colon biopsies revealed overexpression of SLC15A4/PHT1 protein product in the epithelial layer of UC patients. Results were successfully mirrored in vitro, in spontaneously differentiated enterocyte-like monolayers of Caco-2 cells specifically exposed to DSS (dextran sodium sulphate) to mimic IBD inflammatory onsets. SLC15A4/PHT1 expression and cellular localization were characterized confirming its (dys)regulation traits in inflamed vs. healthy epithelia, strongly hinting the hypothesis of SLC15A4/PHT1 increased function associated with epithelial inflammation in IBD patients.