CD66-mediated phagocytosis of Opa52 Neisseria gonorrhoeae requires a Src-like tyrosine kinase- and Rac1-dependent signalling pathway

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Abstract
The interaction of Neisseria gonorrhoeae with human phagocytes is a hallmark of gonococcal infections. Recently, CD66 molecules have been characterized as receptors for Opa52‐expressing gonococci on human neutrophils. Here we show that Opa52‐expressing gonococci or Escherichia coli or F(ab) fragments directed against CD66, respectively, activate a signalling cascade from CD66 via Src‐like protein tyrosine kinases, Rac1 and PAK to Jun‐N‐terminal kinase. The induced signal is distinct from Fcγ‐receptor‐mediated signalling and is specific for Opa52, since piliated Opa− gonococci, commensal Neisseria cinerea or E.coli do not stimulate this signalling pathway. Inhibition of Src‐like kinases or Rac1 prevents the uptake of Opa52 bacteria, demonstrating the crucial role of this signalling cascade for the opsonin‐independent, Opa52/CD66‐mediated phagocytosis of pathogenic Neisseria.