B-1 cells temper endotoxemic inflammatory responses
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2011-03-01
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Barbeiro, Denise Frediani
Barbeiro, Hermes Vieira
Faintuch, Joel
Kubo Ariga, Suely K.
Mariano, Mario [UNIFESP]
Popi, Ana Flavia [UNIFESP]
Souza, Heraldo Possolo de
Velasco, Irineu Tadeu
Soriano, Francisco Garcia
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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.
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Immunobiology. Jena: Elsevier Gmbh, Urban & Fischer Verlag, v. 216, n. 3, p. 302-308, 2011.