| Full text | |
| Author(s): |
Salomao, Reinaldo
[1]
;
Colo Brunialti, Milena Karina
[1]
;
Rapozo, Marjorie Marini
[1]
;
Baggio-Zappia, Giovana Lotici
[1]
;
Galanos, Chris
[2]
;
Freudenberg, Marina
[2]
Total Authors: 6
|
| Affiliation: | [1] Univ Fed Sao Paulo, Escola Paulista Med, Hosp Sao Paulo, Div Infect Dis, Dept Med, Sao Paulo - Brazil
[2] Max Planck Inst Immunobiol, Freiburg - Germany
Total Affiliations: 2
|
| Document type: | Journal article |
| Source: | Shock; v. 38, n. 3, p. 227-242, 2012. |
| Web of Science Citations: | 115 |
| Abstract | |
Since the definition of systemic inflammatory response syndrome/sepsis was originally proposed, a large amount of new information has been generated showing a much more complex scenario of inflammatory and counterinflammatory responses during sepsis. Moreover, some fundamental mechanisms of sensing and destroying invading microorganisms have been uncovered, which include the discovery of TLR4 as the lipopolysaccharide (LPS) gene, implications of innate immune cells as drivers of the adaptive response to infection, and the modulation of multiple accessory molecules that stimulate or inhibit monocyte/macrophage and lymphocyte interactions. The complexity of the infection/injury-induced immune response could be better appreciated with the application of genomics and proteomics studies, and LPS was a useful tool in many of these studies. In this review, we discuss aspects of bacterial recognition and induced cellular activation during sepsis. Because of the relevance of endotoxin (LPS) research in the field, we focus on LPS and host interactions as a clue to understand microorganisms sensing and cell signaling, then we discuss how this response is modulated in septic patients. (AU) | |
| FAPESP's process: | 06/58744-1 - Sepsis: integrating basic research and clinical investigation |
| Grantee: | Reinaldo Salomão |
| Support Opportunities: | Research Projects - Thematic Grants |