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Panminerva Medica 2020 Dec 18

DOI: 10.23736/S0031-0808.20.04205-6

Copyright © 2020 EDIZIONI MINERVA MEDICA

lingua: Inglese

An update on the pathophysiology of acute and recurrent pericarditis

Aldo BONAVENTURA 1, 2, 3 , Alessandra VECCHIÉ 1, 3, Adolfo G. MAURO 1, Antonio L. BRUCATO 4, Massimo IMAZIO 5, Antonio ABBATE 1

1 Virginia Commonwealth University, Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Richmond, VA, USA; 2 First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Genoa, Italy; 3 Internal Medicine Unit, Department of Medicine and Surgery, University of Insubria-Ospedale Di Circolo di Varese, ASST Dei Sette Laghi, Varese, Italy; 4 Department of Biomedical and Clinical Sciences, Fatebenefratelli Hospital, Università di Milano, Milan, Italy; 5 University Cardiology, AOU Città della Salute e della Scienza di Torino, Torino, Italy


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Pericarditis is an inflammatory disease of the pericardium. Progress has been done in recent years in the understanding of its pathophysiology. In particular, pre-clinical and clinical studies have contributed to increasing our knowledge on the role of interleukin (IL)-1 and NLRP3 (NACHT, leucine‐ rich repeat, and pyrin domain‐ containing protein 3) inflammasome. Based on current evidence, pericarditis should be considered as an inflammatory reaction to various stimuli, including chemical/physical, infectious, or ischemic ones, with a viral infection being a common etiology. Interaction of pathogens or irritants with toll-like receptor (TLRs) and stimulation of IL-1 receptor by IL-1α and IL-1β lead to an increased transcription of pro-inflammatory genes, including those needed for NLRP3 inflammasome assembly. This pathway is confirmed indirectly by the beneficial effect of colchicine (an indirect NLRP3 inflammasome inhibitor) and IL-1 blockers in patients with recurrent pericarditis. More recently, a direct evidence of the NLRP3 inflammasome within the inflamed pericardium has been provided as well. It may, however, occur that selfantigens on the surface of mesothelial cells or microbial peptides may stimulate autoreactive T cells along with B cells producing anti-heart antibodies, although less evidence is available on this. Some uncertainties still remain about the role of neutrophils, neutrophil extracellular traps (NETs), and pericardial interstitial cells in recurrent and constrictive pericarditis. Unraveling these aspects might have a direct impact on the development of novel targeted therapies, especially considering the increasing number of drugs targeting NETs.


KEY WORDS: Acute pericarditis; Recurrent pericarditis; IL-1; NLRP3 inflammasome; Autoinflammation; Neutrophils

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