Document Detail


B-1 cells temper endotoxemic inflammatory responses.
MedLine Citation:
PMID:  20817308     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
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-α, 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-α, 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-α, 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.
Authors:
Denise Frediani Barbeiro; Hermes Vieira Barbeiro; Joel Faintuch; Suely K Kubo Ariga; Mario Mariano; Ana Flávia Popi; Heraldo Possolo de Souza; Irineu Tadeu Velasco; Francisco Garcia Soriano
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Publication Detail:
Type:  Journal Article     Date:  2010-08-19
Journal Detail:
Title:  Immunobiology     Volume:  216     ISSN:  1878-3279     ISO Abbreviation:  Immunobiology     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-02-01     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8002742     Medline TA:  Immunobiology     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  302-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier GmbH. All rights reserved.
Affiliation:
Clinical Laboratory in Emergency Medicine, University of São Paulo, School of Medicine, São Paulo, Brazil.
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