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Delivery of Bordetella pertussis adenylate cyclase toxin to target cells via outer membrane vesicles
Author(s) -
Donato Gina M.,
Goldsmith Cynthia S.,
Paddock Christopher D.,
Eby Joshua C.,
Gray Mary C.,
Hewlett Erik L.
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.01.032
Subject(s) - bordetella pertussis , pertussis toxin , cyclase , microbiology and biotechnology , adenylate cyclase toxin , cytochalasin b , cytochalasin d , biology , adenylate kinase , vesicle , g protein , intracellular , receptor , biochemistry , membrane , bacteria , cell , cytoskeleton , genetics
Bordetella pertussis adenylate cyclase toxin (ACT) intoxicates cells by producing intracellular cAMP. B. pertussis outer membrane vesicles (OMV) contain ACT on their surface (OMV–ACT), but the properties of OMV–ACT were previously unknown. We found that B. pertussis in the lung from a fatal pertussis case contains OMV, suggesting an involvement in pathogenesis. OMV–ACT and ACT intoxicate cells with and without the toxin's receptor CD11b/CD18. Intoxication by ACT is blocked by antitoxin and anti‐CD11b antibodies, but not by cytochalasin‐D; in contrast, OMV–ACT is unaffected by either antibody and blocked by cytochalasin‐D. Thus OMV–ACT can deliver ACT by processes distinct from those of ACT alone.