Influence of sera from interstitial lung disease patients on angiogenic activity of mononuclear cells

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Abstract

Chronic inflammation stimulates of neovascularization. The aim of this study was to evaluate the effect of sera from interstitial lung diseases (ILD) patients on angiogenic capabilities of different subsets of mononuclear cells. Serum samples were obtained from 22 patients with sarcoidosis, 20 with hypersensitivity pneumonitis, 20 with idiopathic pulmonary fibrosis, 9 with systemic sclerosis, 6 with pulmonary Langerhans cells histiocytosis, and from 20 healthy volunteers. Animal model of leukocyte induced angiogenesis assay was used as an angiogenic test. The pattern of angiogenic reaction was different in different diseases. Sera from systemic sclerosis and pulmonary Langerhans cells histiocytosis patients exerted inhibitory effects on angiogenesis, but sera from sarcoidosis, hypersensitivity pneumonitis, and idiopathic pulmonary fibrosis patients stimulated angiogenesis. Sera from sarcoidosis and pulmonary Langerhans cells histiocytosis primed monocytes for the production of angiogenic factors. The number of microvessels created after incubation of mononuclear cells depleted of monocytes with sera from systemic sclerosis patients significantly decreased. We conclude that the role of monocytes in the modulation of angiogenesis varies depending on the type of ILD. Sera from sarcoidosis stimulate and from pulmonary Langerhans cells histiocytosis patients inhibit neovascularization induced by monocyte mediators. Sera from systemic sclerosis inhibit angiogenesis induced by lymphocyte products. © 2013 Springer Science+Business Media Dordrecht.

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Zielonka, T. M., Zycinska, K., Radzikowska, E., Filewska, M., Bialas, B., Obrowski, M. H., … Demkow, U. (2013). Influence of sera from interstitial lung disease patients on angiogenic activity of mononuclear cells. In Advances in Experimental Medicine and Biology (Vol. 756, pp. 139–145). Springer Science and Business Media, LLC. https://doi.org/10.1007/978-94-007-4549-0_18

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