• Francisco Garcia Soriano, Hermes Vieira Barbeiro, and Denise Frediani Barbeiro.
• Clinical Emergency, Department of Internal Medicine, Universidade de São Paulo, São Paulo, Brazil.
• Shock. 2013 May 1;39 Suppl 1:5-9.

AbstractInflammation is powerful response to destroy invading organisms, and an exaggerated response can lead to death of the host. Macrophages secrete mediators that activated circulating neutrophils leading to its migration into infectious site. Recently, it has been shown that lymphocytes have an action modulating the early phase of inflammatory response. In this article, we analyze the role of B1 in the inflammatory response of different origins and finally focus attention on sepsis. B lymphocyte deficiency has been linked to acute infection presumably owing to the lack of an adaptive immune response to effectively clear pathogens. Individuals with X-linked agammaglobulinemia (XLA) present B1 lymphocyte deficiency caused by mutations in the Bruton tyrosine kinase (Btk). Some data show that B1 cells might contribute to susceptibility in experimental paracoccidioidomycosis. On the other hand, B1 cells are shown to be detrimental in other mouse models of microbial infection, such as experimental Chagas disease, leishmaniasis, and Staphylococcus aureus-induced arthritis. B1 cell plays a protective role in the host of the effects of endotoxemia. In a murine model of endotoxemia by lipopolysaccharide, B1 cell participates in both interleukin 10 and immunoglobulin M secretion with a consequent reduction in mortality.

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