Loss of hepatic B cells following lipopolysaccharide injection and polymicrobial sepsis

B cells possess pleiotropic functions and are important for both humoral as well as cellular immune responses. However, there is little information about how hepatic B cells respond to lipopolysaccharide (LPS) and/or sepsis. We evaluated the changes in the number of hepatic and splenic B cells, and the expression of immunoglobulins after injecting pathogens, such as LPS, flagellin and CpG oligonucleotides in mice. In addition, we examined the role of natural killer (NK) cells in these changes using mutant bg/bg mice with genetically impaired NK cell functions. Significant temporal loss of hepatic B cells, but not splenic B cells, was seen following LPS treatment. We have shown that bacterial components other than LPS were also responsible for such decline in hepatic B cells. However, loss of hepatic B cells was not seen following LPS treatment in bg/bg mice. In addition, loss of hepatic B cells and systemic immunoglobulin G2a production after LPS treatment was at least in part mediated by interleukin-12, gamma-interferon and tumor necrosis factor-alpha, all of which substantially enhanced the NK cell activity. Hepatic B cells play an essential role during sepsis by synergistically interacting with NK cells. However, whether decline of hepatic B cells after LPS treatment and/or polymicrobial sepsis is simply a phenomenon or has a substantial clinical importance is yet to be determined.