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ORIGINAL ARTICLE   

Minerva Biotecnologica 2020 December;32(4):143-9

DOI: 10.23736/S1120-4826.20.02632-4

Copyright © 2020 EDIZIONI MINERVA MEDICA

lingua: Inglese

Monocyte-derived microparticles stimulate alveolar macrophages from patients with sarcoidosis: modulation by PPARγ

Angela AMORUSO 1, Piero E. BALBO 2, Filippo PATRUCCO 2, 3 , Francesco GAVELLI 3, Luigi M. CASTELLO 3, Claudio BARDELLI 1, Tommaso NERI 4, Alessandro CELI 4, Valentina FOCI 4, Luigia G. FRESU 1, Sandra BRUNELLESCHI 1

1 Department of Health Sciences, Amedeo Avogadro University of Eastern Piedmont, Novara, Italy; 2 Division of Respiratory Medicine, Department of Medicine, Maggiore della Carità University Hospital, Novara Italy; 3 Department of Translational Medicine, Amedeo Avogadro University of Eastern Piedmont, Novara Italy; 4 Department of Surgery, Medical, Molecular, and Critical Area Pathology, University of Pisa, Pisa, Italy



BACKGROUND: Microparticles (MPs) are phospholipid vesicles shed by different cell types during activation or apoptosis, that mediate intercellular communications. Monocyte-derived MPs up-regulate the synthesis of proinflammatory mediators in lung epithelial cells, but their direct effects on human alveolar macrophages (AM) have been never evaluated. Peroxisome Proliferator-activated receptor-gamma (PPARγ) activation usually exerts anti-inflammatory effects, PPARγ agonists showing beneficial effects in experimental models of asthma. In this study we aimed at assessing the ability of monocyte-derived MPs to stimulate AM isolated from patients with sarcoidosis, and the possible modulation by PPARγ.
METHODS: MPs were generated from supernatants of A23187-stimulated human monocytes. AM were challenged by MPs or PMA (used as standard stimulus), in the absence or presence of PPARγ agonists and antagonists, and evaluated for superoxide anion production, cytokine release, nuclear factor (NF)-κB activation and PPARγ expression.
RESULTS: Monocyte-derived MPs induce, in a concentration-dependent manner, oxy-radical production, cytokine release and NF-κB activation in AM, with lower effects than PMA. PPARγ agonists inhibit MPs-induced stimulation, these effects being reversed by the specific antagonist, GW9662. MPs also induce PPARγ protein expression, as do selective agonists.
CONCLUSIONS: In human AM, MPs induce relevant pro-inflammatory effects, that are reduced by PPARγ agonists, but also enhance PPARγ expression, so providing a possible auto-regulatory anti-inflammatory loop.


KEY WORDS: Cell-derived microparticles; Alveolar macrophages; Sarcoidosis; Cytokines; PPAR gamma; Rosiglitazone

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