B Cells Regulate Neutrophilia during Mycobacterium tuberculosis Infection and BCG Vaccination by Modulating the Interleukin-17 Response
Figure 2
B cell-deficiency in μMT mice is associated with an augmented lung Th17 response in tuberculous mice during the acute phase of infection: reversibility of neutrophilia by IL-17 neutralization.
Wild-type or B cell-deficient μMT mice were infected aerogenically with 200–300 CFU of M. tuberculosis Erdman. Lungs cells were procured for cytometric analysis, in conjunction with intracellular staining, at appropriate time intervals p.i.. A, Compared to wild-type C57BL/6s, B cell-deficient μMT mice displayed increased in the number of IL-17A-producing lung cells and B, total number of pulmonic Th17 cells (CD3+CD4+IL-17A+) upon M. tuberculosis infection (*p<0.05). C, Quantification of neutrophil infiltration into the lungs of B cell-deficient μMT mice following IL-17 neutralization at day 14 p.i. revealed that increased neutrophilia was reversed via treatment with a mAb specific for this cytokine (***p<0.0005). D, this reversibility was not due to differences in bacterial burden since the total numbers of CFU in the lungs of mAb-treated and -untreated mouse groups were comparable. Data presented are representative of two to three experiments with three to five mice per group.