Streptococcus pneumoniae pneumolysin and neuraminidase A convert high-density lipoproteins into pro-atherogenic particles
Syed, Shahan; Nissilä, Eija; Ruhanen, Hanna; Fudo, Satoshi; Gaytán, Meztlli O.; Sihvo, Sanna P.; Lorey, Martina B.; Metso, Jari; Öörni, Katariina; King, Samantha J.; Oommen, Oommen P.; Jauhiainen, Matti; Meri, Seppo; Käkelä, Reijo; Haapasalo, Karita (2021)
Syed, Shahan
Nissilä, Eija
Ruhanen, Hanna
Fudo, Satoshi
Gaytán, Meztlli O.
Sihvo, Sanna P.
Lorey, Martina B.
Metso, Jari
Öörni, Katariina
King, Samantha J.
Oommen, Oommen P.
Jauhiainen, Matti
Meri, Seppo
Käkelä, Reijo
Haapasalo, Karita
2021
102535
Julkaisun pysyvä osoite on
https://urn.fi/URN:NBN:fi:tuni-202106145873
https://urn.fi/URN:NBN:fi:tuni-202106145873
Kuvaus
Peer reviewed
Tiivistelmä
High-density lipoproteins (HDLs) are a group of different subpopulations of sialylated particles that have an essential role in the reverse cholesterol transport (RCT) pathway. Importantly, changes in the protein and lipid composition of HDLs may lead to the formation of particles with reduced atheroprotective properties. Here, we show that Streptococcus pneumoniae pneumolysin (PLY) and neuraminidase A (NanA) impair HDL function by causing chemical and structural modifications of HDLs. The proteomic, lipidomic, cellular, and biochemical analysis revealed that PLY and NanA induce significant changes in sialic acid, protein, and lipid compositions of HDL. The modified HDL particles have reduced cholesterol acceptor potential from activated macrophages, elevated levels of malondialdehyde adducts, and show significantly increased complement activating capacity. These results suggest that accumulation of these modified HDL particles in the arterial intima may present a trigger for complement activation, inflammatory response, and thereby promote atherogenic disease progression.
Kokoelmat
- TUNICRIS-julkaisut [16929]