Our study reveals a previously unrecognized role for the PRR, PGLYRP1, in orchestrating both antibacterial defenses and inflammatory responses during B. pertussis infection. This is comparable to SIGLECs, which can distinguish self from non-self glycans to ignore or elicit immune responses (Paulson et al., 2012). During B. pertussis infection, PGLYRP1, predominantly expressed by neutrophils, contributes to early bacterial clearance, as PGLYRP1 KO mice exhibit significantly higher bacterial loads at 4DPI. These data suggest B. pertussis may exploit PGLYRP1 to amplify a NOD1-dominant signaling environment that blunts host inflammation. We hypothesize that B. pertussis may attenuate host immune responses not merely by evading recognition, but by actively hijacking host regulatory circuits through the release of specific PGN structures.