FIG 1.
Hematopoietic MyD88 signaling mediates both inflammation and control of Brucella joint infection. (A) MyD88fl/fl (control) and hematopoietic MyD88-deficient (MyD88fl/fl-Vav1cre) mice (n = 4 to 6/group) were infected in both rear footpads with 1 × 105 B. melitensis 16M, and joint swelling was measured over time. (B) MyD88fl/fl-Vav1cre or control animals (WT or MyD88fl/fl) (n = 4 to 8/group) were infected in both rear footpads with 1 × 105 B. melitensis 16M, and colonization of the joint by Brucella was determined at 2, 7, or 37 days postinfection. *, P < 0.05 compared to control mice (WT or MyD88fl/fl). Error bars depict standard deviations (SD) from the means. Data are representative of 2 independent experiments. ns, not significant.