SummaryThe local cytokine environment and presence of stimulatory signals determine whether monocytes acquire dendritic cell (DC) or macrophage characteristics and functions. Because enhanced platelet activation is reported in patients with many allergic disorders, such as atopic dermatitis, plateletderived factors may influence monocytic differentiation into DC. In this study we examined the effect of serotonin, a prototypic mediator of allergic inflammation released mainly by activated platelets at the inflammatory site, on the granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-4-driven differentiation of monocytes into monocyte-derived DC. Monocytes from healthy adult donors were cultured with GM-CSF and IL-4 in the presence or absence of serotonin, and the phenotypes and function of these cells were analysed. In the presence of serotonin, monocytes differentiated into DC with reduced expression of co-stimulatory molecules and CD1a, whereas expression of CD14 was increased. These serotonin-treated DC exhibited significantly reduced stimulatory activity toward allogeneic T cells. However, these cells showed enhanced cytokine-producing capacity, including IL-10 but not IL-12. There was no significant difference between both types of DC in phagocytic activity. Experiments using agonists and antagonists indicated that serotonin 5-hydroxytryptamine (5-HT) induced the alteration of their phenotype and reduction in antigen-presenting capacity were mediated via 5-HTR1/7. It is therefore suggested that serotonin-driven DC may have a regulatory function in the inflammatory process.

Low-power laser analgesic effect was generally accepted in clinical cases, whereas there was no direct evidence to indicate that low-power laser irradiation suppressed an impulse conduction within a peripheral nerve. The effect of low-power laser irradiation on electrically evoked responses within the sural nerve was electrophysiologically analyzed in anesthetized rabbits. High threshold evoked responses (conduction velocity was about 11 m/sec, unmyelinated A delta), which were induced by an electrical stimulation to the peripheral stump of the nerve, were significantly suppressed (9 to 19% inhibition) during low-power laser irradiation, which applied to the exposed sural nerve between the stimulus site and the recording site. The suppressive effect was reversible and recovered to the control level after the irradiation. Experimental evidence indicated that low-power laser irradiation suppressed the impulse conduction of unmyelinated A delta afferents in peripheral sensory nerve, which caused a pain sensation. Our data suggest that low-power laser acts as a reversible direct suppressor of neuronal activity.

Summary LIGHT [the name of which is derived from ‘homologous to lymphotoxins, exhibits inducible expression, competes with herpes simplex virus glycoprotein D for herpes simplex virus entry mediator (HVEM), and expressed by T lymphocytes’], is a member of the tumour necrosis factor superfamily that is involved in various inflammatory diseases. We aimed to estimate the relevance of plasma LIGHT levels as a biomarker for atopic dermatitis (AD). In order to understand the putative role of LIGHT in AD pathogenesis, we also investigate the effects of LIGHT on a monocytic cell line, human acute monocytic leukaemia cell line (THP‐1). We examined plasma LIGHT levels, total serum IgE, serum value of CCL17 and peripheral blood eosinophil counts in patients with AD and healthy subjects. The effects of LIGHT on activation and apoptosis in THP‐1 cells were also investigated. The plasma concentrations of LIGHT in AD patients were significantly higher than those in healthy individuals and the concentrations decreased as the symptoms were improved by treatment. The LIGHT plasma concentrations correlated with IgE levels and the Severity Scoring of AD (SCORAD) index. In addition, LIGHT stimulation increased expression of CD86 and induced production of interleukin‐1β in THP‐1 cells. Apoptosis was inhibited, the Bcl‐2 level increased and the caspase‐3 level decreased in THP‐1 cells stimulated with LIGHT, compared to unstimulated control cells. These results suggest that plasma LIGHT levels may be one of the promising biomarkers for AD.

The conflicting views of the effect of low-power laser (LPL) irradiation on procollagen synthesis have existed at the present time, whereas many clinical studies have tested usefulness of LPL irradiation for the wound healing. To evaluate the effect of LPL irradiation on the procollagen synthesis of human fibroblasts in vitro, LPL irradiation on human fibroblast was carried out using two different culture medium, serum-starved medium and fetal calf serum (FCS)-contained medium. In addition, to investigate the mechanism of the LPL on the procollagen synthesis of human fibroblasts, dexamethasone and methylene blue contained medium were used for inhibition of procollagen product at the pretranslational level and cGMP-mediated processes, respectively. Enhanced effect of LPL was consistently observed in the serum-starved medium (50% increase by a 3 min irradiation), not in the FCS-contained medium. The LPL enhanced effect was not blocked by dexamethasone (3% inhibition) but methylene blue (40% inhibition). Our data suggest that some factors in FCS might interfere with the enhanced effect of LPL on procollagen synthesis and the LPL might act as a direct stimulator of the procollagen synthesis. It seems probable that the LPL enhanced effects might be occurred at the translational level or at the pretranslational level, which is not affected by dexamethasone and cGMP, might be involved in the LPL enhanced effect of the procollagen synthesis in fibroblast.

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