Pentraxin-3-mediated complement activation in a swine model of renal ischemia/reperfusion injury
Chiara Divella, Alessandra Stasi, Rossana Franzin, Michele Rossini, Paola Pontrelli, Fabio Sallustio, Giuseppe Stefano Netti, Elena Ranieri, Luca Lacitignola, Francesco Staffieri, Alberto Maria Crovace, Giuseppe Lucarelli, Pasquale Ditonno, Michele Battaglia, Mohamed R. Daha, P. van der Pol, Cees van Kooten, Giuseppe Grandaliano, Loreto Gesualdo, Giovanni Stallone, Giuseppe Castellano
Abstract
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.