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  • Title: Neutrophil respiratory burst is decreased in scleroderma and normalized by near-infrared mediated hyperthermia.
    Author: Foerster J, Storch A, Fleischanderl S, Wittstock S, Pfeiffer S, Riemekasten G, Worm M.
    Journal: Clin Exp Dermatol; 2006 Nov; 31(6):799-806. PubMed ID: 16939588.
    Abstract:
    BACKGROUND: The production of reactive oxygen species (ROS) by fibroblasts has been suggested to contribute to scleroderma pathogenesis. Infrared-mediated hyperthermia has recently been shown to be of benefit in scleroderma. AIM: As the contribution of neutrophils and monocytes to ROS formation in scleroderma is unknown, we studied respiratory burst in these cell types. We also aimed to test the hypothesis that near-infrared (IRA) treatment may effect burst activity. METHODS: We determined respiratory burst in patients with scleroderma (n = 22) and age- and sex-matched controls (n = 20) at baseline, and after high-level stimulation by phorbolmyristyl acetate (PMA) and low-level stimulation by non-opsonized zymosan. Respiratory burst was also assessed before and after a series of infrared-mediated hyperthermia treatments. RESULTS: Unexpectedly, we observed no increase but instead a slight but statistically significant reduction in baseline and zymosan-stimulated respiratory burst in scleroderma neutrophils (P < 0.001) and monocytes (P < 0.005). This decrease in burst activity was nonspecific, as it was also observed in patients with another active inflammatory disease, psoriasis. IRA treatment induced a cell-type-specific normalization of respiratory burst only in neutrophils, but not in monocytes. Intriguingly, neutrophil-specific normalization of ROS formation persisted for 6 weeks after the end of IRA treatment, in concordance with the previously reported clinical responses to this therapy. CONCLUSION: Neutrophils and monocytes do not exhibit cell-autonomous overproduction of ROS in scleroderma, thereby implicating fibroblasts as main source for clinically relevant ROS accumulation. Furthermore, repeated mild infrared-mediated hyperthermia exerts a lasting cell-type-specific effect on neutrophils.
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