B-1 cells temper endotoxemic inflammatory responses

B-1 cells temper endotoxemic inflammatory responses

Author Barbeiro, Denise Frediani Google Scholar
Barbeiro, Hermes Vieira Google Scholar
Faintuch, Joel Google Scholar
Kubo Ariga, Suely K. Google Scholar
Mariano, Mario Autor UNIFESP Google Scholar
Popi, Ana Flavia Autor UNIFESP Google Scholar
Souza, Heraldo Possolo de Google Scholar
Velasco, Irineu Tadeu Google Scholar
Soriano, Francisco Garcia Google Scholar
Institution Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Abstract Sepsis syndrome is caused by inappropriate immune activation due to bacteria and bacterial components released during infection. This syndrome is the leading cause of death in intensive care units. Specialized B-lymphocytes located in the peritoneal and pleural cavities are known as B-1 cells. These cells produce IgM and IL-10, both of which are potent regulators of cell-mediated immunity. It has been suggested that B-1 cells modulate the systemic inflammatory response in sepsis. in this study, we conducted in vitro and in vivo experiments in order to investigate a putative role of B-1 cells in a murine model of LPS-induced sepsis. Macrophages and B-1 cells were studied in monocultures and in co-cultures. the B-1 cells produced the anti-inflammatory cytokine IL-10 in response to LPS. in the B-1 cell-macrophage co-cultures, production of proinflammatory mediators (TNF-alpha, IL-6 and nitrite) was lower than in the macrophage monocultures, whereas that of IL-10 was higher in the co-cultures. Co-culture of B-1 IL-10(-/-) cells and macrophages did not reduce the production of the proinflammatory mediators (TNF-alpha, IL-6 and nitrite). After LPS injection, the mortality rate was higher among Balb/Xid mice, which are B-1 cell deficient, than among wild-type mice (65.0% vs. 0.0%). the Balb/Xid mice also presented a proinflammatory profile of TNF-alpha, IL-6 and nitrite, as well as lower levels of IL-10. in the early phase of LPS stimulation, B-1 cells modulate the macrophage inflammatory response, and the main molecular pathway of that modulation is based on IL-10-mediated intracellular signaling. (C) 2010 Elsevier GmbH. All rights reserved.
Keywords Cytokines
Language English
Date 2011-03-01
Published in Immunobiology. Jena: Elsevier Gmbh, Urban & Fischer Verlag, v. 216, n. 3, p. 302-308, 2011.
ISSN 0171-2985 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 302-308
Origin http://dx.doi.org/10.1016/j.imbio.2010.08.002
Access rights Closed access
Type Article
Web of Science ID WOS:000288722500004
URI http://repositorio.unifesp.br/handle/11600/33526

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