Infection of B cell-deficient mice with CDC 1551, a clinical isolate of Mycobacterium tuberculosis: Delay in dissemination and development of lung pathology

Long-term survival of mice infected with Mycobacterium tuberculosis is depe ndent upon IFN-gamma and T cells, but events in early phases of the immune response are not well, understood, In this study, we describe a role for B cells during early immune responses to infection with a clinical isolate of M. tuberculosis (CDC 1551), Following a low-dose infection with M. tubercu losis CDC 1551, similar numbers of bacteria were detected in the lungs of b oth B cell knockout (IgH 6(-), BKO) and C57BL/6J (wild-type) mice. However, despite comparable bacterial loads in the lungs, less severe pulmonary gra nuloma formation and delayed dissemination of bacteria from lungs to periph eral organs were observed in BKO mice. BKO mice reconstituted with naive B cells, but not those given M, tuberculosis-specific Abs, before infection d eveloped pulmonary granulomas and dissemination patterns similar to wildtyp e animals. Further analysis of lung cell populations revealed greater numbe rs of lymphocytes, especially CD8(+) T cells, macrophages, and neutrophils in wild-type and reconstituted mice than in BKO mice. Thus, less severe les ion formation and delayed dissemination of bacteria found in BKO mice were dependent on B cells, not Abs, and were associated with altered cellular in filtrate to the lungs. These observations demonstrate an important, previou sly unappreciated, role for B cells during early immune responses to M. tub erculosis infections.