Hemorrhage in mice produces alterations in B cell repertoires.

Multiple organ system failure secondary to infection is the major cause of late deaths after trauma and hemorrhage. The production by B cells of antibodies directed against bacterial antigens is an important component of host defenses. In order to determine the effects of hemorrhage on B cell function, we examined hemorrhage-induced alterations in available (clonal precursors) and actual (plasma cells) B cell repertoires in the course of an immune response toward bacterial antigens. Hemorrhage produced greater than twofold decreases in the absolute frequency and number of clonal precursors specific for the bacterial antigens dextran, levan, and pneumococcal polysaccharide type II. After blood loss, there were decreases in absolute frequency, but not in numbers, of clonal precursors capable of producing antibodies against the nonbacterial antigens ovalbumin and mouse transferrin. Immunization with the bacterial antigen levan within 24 hr of hemorrhage resulted in approximately 50% fewer levan-specific plasma cells than that seen in normal, unhemorrhaged mice. These results demonstrate that hemorrhage produces marked alterations in B cell repertoires, which may contribute to postinjury abnormalities in host defenses.