As shown in Fig. 3B, compared to mock-treated cells (control), or the monocytes infected by the B. pertussis (AC−PT+) mutant producing active PT and the enzymatically inactive CyaA-AC− toxoid (Table 1), which differentiated and expressed higher levels of CD71 and CD163 (Fig. 3B and C), monocyte infection with the wild-type B. pertussis strain producing both toxins (AC+PT+) provoked a significant decrease in the number of cells that still expressed some CD71 and CD163 receptor on cell surface. Here, CD163 is linked to infection.