Details

Autor(en) / Beteiligte

• Divella, Chiara
• Stasi, Alessandra
• Franzin, Rossana
• Rossini, Michele
• Pontrelli, Paola
• Sallustio, Fabio
• Netti, Giuseppe Stefano
• Ranieri, Elena
• Lacitignola, Luca
• Staffieri, Francesco
• Crovace, Alberto Maria
• Lucarelli, Giuseppe
• Ditonno, Pasquale
• Battaglia, Michele
• Daha, Mohamed R
• van der Pol, Peter
• van Kooten, Cees
• Grandaliano, Giuseppe
• Gesualdo, Loreto
• Stallone, Giovanni
• Castellano, Giuseppe

Titel

Pentraxin-3-mediated complement activation in a swine model of renal ischemia/reperfusion injury

Ist Teil von

• Aging (Albany, NY.), 2021-04, Vol.13 (8), p.10920-10933

Ort / Verlag

United States: Impact Journals

Erscheinungsjahr

2021

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• Pentraxins are a family of evolutionarily conserved pattern recognition molecules with pivotal roles in innate immunity and inflammation, such as opsonization of pathogens during bacterial and viral infections. In particular, the long Pentraxin 3 (PTX3) has been shown to regulate several aspects of vascular and tissue inflammation during solid organ transplantation. Our study investigated the role of PTX3 as possible modulator of Complement activation in a swine model of renal ischemia/reperfusion (I/R) injury. We demonstrated that I/R injury induced early PTX3 deposits at peritubular and glomerular capillary levels. Confocal laser scanning microscopy revealed PTX3 deposits co-localizing with CD31 endothelial cells. In addition, PTX3 was associated with infiltrating macrophages (CD163), dendritic cells (SWC3a) and myofibroblasts (FSP1). In particular, we demonstrated a significant PTX3-mediated activation of classical (C1q-mediated) and lectin (MBL-mediated) pathways of Complement. Interestingly, PTX3 deposits co-localized with activation of the terminal Complement complex (C5b-9) on endothelial cells, indicating that PTX3-mediated Complement activation occurred mainly at the renal vascular level. In conclusion, these data indicate that PTX3 might be a potential therapeutic target to prevent Complement-induced I/R injury.