CX3CL1 and respiratory tract infectious disorder: Our study is the first to show that S. aureus induces shedding of CX3CL1 by lung epithelial cells via α-toxin-mediated cytotoxicity and activation of ADAM10, with the potential to modulate immune responses locally and impair monocytes’ antimicrobial function, thereby contributing toward S. aureus pathogenesis and survival during respiratory infections.