Inflammation is powerful response in order 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 has been showing that lymphocytes have an action modulating the early phase of inflammatory response. In this article we will 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 adaptative immune response to effectively clear pathogens. Individuals with X-linked agammaglobulinemia (XLA) present B-1 lymphocyte deficiency caused by mutations in the Bruton's tyrosine kinase (Btk). Some data show that B-1 cells might contribute to susceptibility in experimental paracoccidioidomycosis. On the other hand, B-1 cells are shown to be detrimental in other mouse models of microbial infection, such as experimental Chagas' disease, leishmaniasis and Staphylococcus aureus-induced arthritis. B-1 cell plays a protective role in the host of the effects of endotoxemia. In a murine model of endotoxemia by LPS, B-1 cell participates in both IL-10 and IgM secretion with a consequent reduction in mortality.