: Chronic immune activation is the key pathogenetic event of Mycobacterium tuberculosis (MTB) and human immunodeficiency virus (HIV) coinfection. In the present study, we have assessed the therapeutic value of phosphatidylserine-liposome (PS-L) in an in vitro model of MTB/HIV coinfection. Our results show that PS-L reduce NF-κB activation and the downstream production of TNF-α, IL-1β and IL-6 in BCG-infected macrophages and of TNF-α and IL-1β in MTB-infected and in MTB/HIV-coinfected macrophages. Importantly, a significant reduction of intracellular MTB viability and HIV replication were also observed. These results support the further exploitation of PS-L as a host directed therapy for MTB/HIV coinfection.
Poerio, N., Caccamo, N., La Manna, M.p., Olimpieri, T., Henrici De Angelis, L., D'Andrea, M.m., et al. (2021). Phosphatidylserine liposomes reduce inflammatory response, mycobacterial viability and HIV replication in coinfected human macrophages. THE JOURNAL OF INFECTIOUS DISEASES [10.1093/infdis/jiab602].
Phosphatidylserine liposomes reduce inflammatory response, mycobacterial viability and HIV replication in coinfected human macrophages
Poerio, N;D'Andrea, M M;Fraziano, M
2021-12-15
Abstract
: Chronic immune activation is the key pathogenetic event of Mycobacterium tuberculosis (MTB) and human immunodeficiency virus (HIV) coinfection. In the present study, we have assessed the therapeutic value of phosphatidylserine-liposome (PS-L) in an in vitro model of MTB/HIV coinfection. Our results show that PS-L reduce NF-κB activation and the downstream production of TNF-α, IL-1β and IL-6 in BCG-infected macrophages and of TNF-α and IL-1β in MTB-infected and in MTB/HIV-coinfected macrophages. Importantly, a significant reduction of intracellular MTB viability and HIV replication were also observed. These results support the further exploitation of PS-L as a host directed therapy for MTB/HIV coinfection.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.