ATTACHMENT OF PILIATED, OPA(-) AND OPC(-) GONOCOCCI AND MENINGOCOCCI TO EPITHELIAL-CELLS ELICITS CORTICAL ACTIN REARRANGEMENTS AND CLUSTERING OF TYROSINE-PHOSPHORYLATED PROTEINS

Attachment of piliated Neisseria gonorrhoeae or Neisseria meningitidis cells to A431, hang, HEC-1-B, or polarized T-84 cells triggers rearra ngements of cortical microfilaments and the accumulation of phosphotyr osine-containing proteins at sites of bacterial contact. Actin stress fibers and the microtubule network remain unaltered in infected cells. The rearrangements reported here are triggered by piliated, Opa-and O pe-strains and also by nonpiliated gonococci (GC) that produce the inv asion-associated OpaA protein. Thus, neisserial adhesion via either of at least two different adhesins can trigger cortical rearrangements. In contrast, these rearrangements are not triggered by nonadherent GC or meningococcal strains, by heat-killed or chloramphenicol-treated GC strains, or by Escherichia coli recombinants that adhere to cells via GC OpaA or Opal fusion proteins, suggesting that additional neisseria l components are involved. Immunoblotting experiments did not detect c onsistent increases in the phosphorylation of specific proteins. Possi ble biological implications of these Neisseria-induced cortical rearra ngements are discussed.