pneumoniae</i> remains poorly understood; In this study, we constructed a <i>crp</i> deletion mutant (Δ<i>crp</i>) and a complemented strain (c-Δ<i>crp</i>) and employed a combination of in vitro virulence assays, in vivo infection models, transcriptomic profiling, and functional metabolic analyses to dissect the CRP-mediated metabolism-virulence regulatory axis; We show that <i>crp</i> deficiency does not significantly alter susceptibility to clinically relevant antibiotics but markedly impairs biofilm formation, motility, and host cell adhesion and invasion. This evidence concerns the gene CRP and infection.