| Full text | |
| Author(s): Show less - |
Ferreira, Raphael G.
[1]
;
Rodrigues, Lilian C.
[2]
;
Nascimento, Daniele C.
[1]
;
Kanashiro, Alexandre
[1]
;
Melo, Paulo H.
[1]
;
Borges, Vanessa F.
[1]
;
Gozzi, Aline
[3]
;
Prado, Douglas da Silva
[1]
;
Borges, Marcos C.
[3]
;
Ramalho, Fernando S.
[4]
;
Stowell, Sean R.
[5]
;
Cummings, Richard D.
[6]
;
Dias-Baruffi, Marcelo
[2]
;
Cunha, Fernando Q.
[1]
;
Alves-Filho, Jose C.
[1]
Total Authors: 15
|
| Affiliation: | [1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Sch Pharmaceut Sci Ribeirao Preto, Dept Clin Anal Toxicol & Food Sci, Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Internal Med, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pathol, Ribeirao Preto, SP - Brazil
[5] Emory Univ, Dept Pathol, Sch Med, Atlanta, GA 30322 - USA
[6] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Surg, Boston, MA - USA
Total Affiliations: 6
|
| Document type: | Journal article |
| Source: | Journal of Infection; v. 77, n. 5, p. 391-397, NOV 2018. |
| Web of Science Citations: | 4 |
| Abstract | |
Sepsis is an overwhelming systemic inflammation resulting from an uncontrolled infection that causes extensive tissue damage, organ dysfunction and eventually death. A growing body of evidence indicates that impaired neutrophil migration to the site of infection is associated with poor outcome in sepsis. Here we show that galectin-3 (Gal-3), an endogenous glycan-binding protein, plays a critical role in sepsis outcome. We found that serum Gal-3 concentration increased in patients with septic shock and mice undergoing sepsis induced by cecal ligation and puncture (CLP). Mice deficient in Gal-3 (Gal-3 KO) are more resistant to sepsis induced by CLP, showing lower levels of biochemical markers and neutrophil infiltration for organ injury/dysfunction than those observed in wild-type mice (WT). Furthermore, Gal-3 KO mice show an increased number of neutrophils in the primary focus of infection and reduced bacterial loads in the peritoneal cavity, blood, and lungs. Mechanistically, blood neutrophils from septic mice show higher levels of surface-bound Gal-3 than neutrophils from naive mice. The deficiency of Gal-3 was associated with increased rolling and adhesion of these cells in mesenteric venules. Our results indicate that Gal-3, secreted during sepsis, inhibits neutrophil migration into the infectious focus, which promotes the bacterial spread and worsens the outcome of sepsis. (C) 2018 The British Infection Association. Published by Elsevier Ltd. All rights reserved. (AU) | |
| FAPESP's process: | 13/08216-2 - CRID - Center for Research in Inflammatory Diseases |
| Grantee: | Fernando de Queiroz Cunha |
| Support Opportunities: | Research Grants - Research, Innovation and Dissemination Centers - RIDC |
| FAPESP's process: | 11/19670-0 - Mechanisms involved in the pathophysiology of rheumatoid arthritis, pain and sepsis |
| Grantee: | Fernando de Queiroz Cunha |
| Support Opportunities: | Research Projects - Thematic Grants |