A deficient humoral immune response may be originated in alterations at different levels of the development of B cells. In the case of an infection, a deficient humoral response has strong consequences in the control of the microorganism replication and in the development of the pathology. The acute phase of Trypanosoma cruzi infection is characterized by an extensive polyclonal activation of B cells that coexists with a humoral immunosuppressive state and an enhanced apoptosis of B cells. We investigate the influence of T. cruzi infection on the central B cell compartment. We observed that mice ongoing the acute phase of T. cruzi infection present a marked cellular hypoplasia in bone marrow, which mainly affects immature B220^lowHSA^high B cells. We found that splenic immature B lymphocytes are also reduced, indicating that an exacerbated progenitor migration to periphery is not responsible for the hypoplasia in the bone marrow. The percentage of CD19⁺ B cells with hypo-diploid nuclei in the bone marrow from acute infected mice is higher than in that from normal mice, revealing that the infection increase the rate of apoptosis. Even though the bone marrow hypoplasia is transient and coincident with the presence of parasite in blood, the cell death is not a direct effect of parasite-cell interaction, since incubation of normal bone marrow cells with trypomastigotes from T. cruzi does not result in B cell apoptosis. By co-cultures, we demonstrated that bone marrow cells from infected mice secrete a soluble factor which eliminates immature B cells. We also show that this factor is not IFN- , TGF- or H₂O₂ but it is a product of the ciclooxigenase pathway since indomethacin treatment is able to restrain the apoptosis induced by bone marrow from infected mice. Finally, we show that infected bone marrow depleted from Mac⁺, but not Thy1.2⁺, cells was unable to induce immature B cell elimination, indicating a pivotal role of myeloid cells in B cell hypoplasia. These findings indicate that the Trypanosoma cruzi infection induces myeloid cells to secrete a product of the ciclooxigenase pathway that eliminates immature B cells, affecting the progression of the effector humoral response.