The Gram-negative bacterium Neisseria meningitidis causes meningitis in humans and has been demonstrated to manipulate or alter host signalling pathways during infection of the central nervous system. In this study, the phosphoproteome of an in vitro model of the blood-cerebrospinal fluid barrier was investigated during infection with the Neisseria meningitidis serogroup B (NmB) strain MC58 in presence and absence of the bacterial capsule. We show that the capsule deficient mutant has a higher impact on the phosphoproteome of the infected cells and identify potentially regulated pathways and cellular processes during infection.