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Galectin-3 Aggravates Experimental Polymicrobial Sepsis by Impairing Neutrophil Recruitment to the Infectious Focus
Jun. 10, 2018- By: Raphael G Ferreira;Lilian C Rodrigues;Daniele C Nascimento;Alexandre Kanashiro;Paulo H Melo;Vanessa F Borges;Aline Gozzi;Douglas da Silva Prado;Marcos C Borges;Richie Purseglove
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- Serum Gal-3 concentration increased in patients with septic shock and mice undergoing sepsis induced by a procedure called cecal ligation and puncture (CLP).
- Mice genetically deficient in Gal-3 (Gal-3 KO) were more resistant to sepsis caused by CLP than wild-type mice (WT).
- Gal-3 KO mice show an increased number of neutrophils in the initial stage of infection and reduced bacterial loads in the peritoneal cavity and blood.
- Blood neutrophils from septic mice show higher levels of surface-bound Gal-3 than neutrophils from control mice.
- Results indicate that Gal-3, secreted during sepsis, inhibits neutrophil migration into the infectious site, promoting the bacterial spread.
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