TY - JOUR
T1 - Histotoxic clostridial infections
AU - Nagahama, Masahiro
AU - Takehara, Masaya
AU - Rood, Julian I.
PY - 2019/7
Y1 - 2019/7
N2 - The pathogenesis of clostridial myonecrosis or gas gangrene involves an interruption to the blood supply to the infected tissues, often via a traumatic wound, anaerobic growth of the infecting clostridial cells, the production of extracellular toxins, and toxin-mediated cell and tissue damage. This review focuses on host-pathogen interactions in Clostridium perfringens-mediated and Clostridium septicum-mediated myonecrosis. The major toxins involved are C. perfringens α-toxin, which has phospholipase C and sphingomyelinase activity, and C. septicum α-toxin, a β-pore-forming toxin that belongs to the aerolysin family. Although these toxins are cytotoxic, their effects on host cells are quite complex, with a range of intracellular cell signaling pathways induced by their action on host cell membranes.
AB - The pathogenesis of clostridial myonecrosis or gas gangrene involves an interruption to the blood supply to the infected tissues, often via a traumatic wound, anaerobic growth of the infecting clostridial cells, the production of extracellular toxins, and toxin-mediated cell and tissue damage. This review focuses on host-pathogen interactions in Clostridium perfringens-mediated and Clostridium septicum-mediated myonecrosis. The major toxins involved are C. perfringens α-toxin, which has phospholipase C and sphingomyelinase activity, and C. septicum α-toxin, a β-pore-forming toxin that belongs to the aerolysin family. Although these toxins are cytotoxic, their effects on host cells are quite complex, with a range of intracellular cell signaling pathways induced by their action on host cell membranes.
UR - http://www.scopus.com/inward/record.url?scp=85070470562&partnerID=8YFLogxK
U2 - 10.1128/microbiolspec.GPP3-0024-2018
DO - 10.1128/microbiolspec.GPP3-0024-2018
M3 - Article
C2 - 31350831
AN - SCOPUS:85070470562
VL - 7
JO - Microbiology Spectrum
JF - Microbiology Spectrum
SN - 2165-0497
IS - 4
M1 - GPP3-0024-2018
ER -