Open AccessTrimeresurus flavoviridis (Habu Snake) Venom Induces Human Erythrocyte Lysis through Enzymatic Lipolysis, Complement Activation and Decreased Membrane Expression of CD55 and CD59
Author(s) -
Yamamoto Chieko,
Tsuru Daisuke,
OdaUeda Naoko,
Ohno Motonori,
Hattori Shosaku,
Kim SungTeh
Publication year - 2001
Publication title -
pharmacology & toxicology
Language(s) - English
Resource type - Journals
eISSN - 1600-0773
pISSN - 0901-9928
DOI - 10.1111/j.0901-9928.2001.890408.x
Subject(s) - cd59 , haemolysis , venom , complement system , complement membrane attack complex , hemolysis , snake venom , lysis , biology , biochemistry , decay accelerating factor , red blood cell , microbiology and biotechnology , chemistry , immune system , immunology
Trimeresurus flavoviridis (habu snake) bites can be fatal to man because of its virulent venom, which is clinicopathologically classified as haemorrhagic, necrotic, and haemolytic toxins. Trimeresurus flavoviridis venom causes lysis of human erythrocytes in conditions where plasma is present as well as in plasma‐free conditions in a dose‐dependent manner. The haemolytic process requires Ca 2+ and Mg 2+ ions in the solution. Additionally, the venom initiates activation of the human complement cascade as evidenced by C3a and C5a releases, complement consumption indicated by CH50 and formation of soluble membrane attack complex. The insertion of membrane attack complex into the erythrocyte membranes is morphologically identified by electronmicroscopy. Immunofluorescence analysis reveals that incubation of erythrocytes with the venom decreased cell‐surface expression of CD55 (decay accelerating factor) and CD59 (protectin), which renders erythrocyte more vulnerable to adherent C3 and C5 convertases and to polymerization of C9 into membranes, and may enhance autologous complement‐mediated haemolysis triggered by the venom. Our data demonstrate that Trimeresurus flavoviridis venom induces haemolysis in the presence of plasma by three distinct mechanisms, direct lipolysis through PLA 2 activity, activation of the human complement system, and cleavages of CD55 and CD59 from erythrocyte membranes.