The omentum is a site of IgM production during T cell-independent bacterial infection in secondary lymphoid organ-deficient mice (43.6)

Abstract

Abstract Infection of mice with the bacterium Ehrlichia muris results in a T cell-independent (TI) splenic IgM response, and this antibody is secreted largely by a population of CD11c-expressing B cell plasmablasts in the spleen. However, we found that the TI IgM is maintained in the absence of a spleen; infection of splenectomized mice resulted in a modest decrease in antigen-specific serum IgM, indicating that splenic B cells are not required for the generation of the protective antibody response. To identify the source of the IgM-secreting cells, we infected secondary lymphoid organ (SLO)-deficient mice, which lack both spleen and lymph nodes. SLO-deficient mice were similarly able to produce ehrlichia-specific IgM, and both splenectomized and SLO-deficient mice were protected against challenge infection with a lethal ehrlichial species. These findings led us to investigate the omentum as a source of IgM-secreting cells during infection. We identified the omentum as a large reservoir of antigen-specific IgM-secreting cells; these B cells expressed CD11c, but lacked expression of CD138. CD11c-expressing B cells were elicited by intraperitoneal, but not intravenous infection, revealing a route-dependent response to peritoneal antigen. Our data reveal the omentum as an important site of TI IgM production against peritoneal antigens, in the absence of conventional secondary lymphoid organs.