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Distinct mechanisms of internalization of Neisseria gonorrhoeae by members of the CEACAM receptor family involving Rac1- and Cdc42-dependent and -independent pathways
Max‐Planck‐Institut für Infektionsbiologie, Abteilung Molekulare Biologie, Schumannstraße 21/22, D‐10117 Berlin, Germany.ORCID iD: 0000-0003-1716-168x
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2002 (English)In: EMBO Journal, ISSN 0261-4189, E-ISSN 1460-2075, Vol. 21, no 4, p. 560-571Article in journal (Refereed) Published
Abstract [en]

Opa adhesins of pathogenic Neisseria species target four members of the human carcinoembryonic antigen-related cellular adhesion molecule (CEACAM) family. CEACAM receptors mediate opsonization-independent phagocytosis of Neisseria gonorrhoeae by human granulocytes and each receptor individually can mediate gonococcal invasion of epithelial cells. We show here that gonococcal internalization occurs by distinct mechanisms depending on the CEACAM receptor expressed. For the invasion of epithelial cell lines via CEACAM1 and CEACAM6, a pathogen-directed reorganization of the actin cytoskeleton is not required. In marked contrast, ligation of CEACAM3 triggers a dramatic but localized reorganization of the host cell surface leading to highly efficient engulfment of bacteria in a process regulated by the small GTPases Rac1 and Cdc42, but not Rho. Two tyrosine residues of a cytoplasmic immune receptor tyrosine-based activating motif of CEACAM3 are essential for the induction of phagocytic actin structures and subsequent gonococcal internalization. The granulocyte-specific CEACAM3 receptor has properties of a single chain phagocytic receptor and may thus contribute to innate immunity by the elimination of Neisseria and other CEACAM-binding pathogens that colonize human mucosal surfaces.

Place, publisher, year, edition, pages
European Molecular Biology Organization , 2002. Vol. 21, no 4, p. 560-571
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Cell and Molecular Biology
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URN: urn:nbn:se:umu:diva-165895DOI: 10.1093/emboj/21.4.560PubMedID: 11847104OAI: oai:DiVA.org:umu-165895DiVA, id: diva2:1379098
Available from: 2019-12-16 Created: 2019-12-16 Last updated: 2019-12-18Bibliographically approved

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Billker, Oliver

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