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Structure-Function Relationships Underlying the Capacity of Bordetella Adenylate Cyclase Toxin to Disarm Host Phagocytes

J. Novak, O. Cerny, A. Osickova, I. Linhartova, J. Masin, L. Bumba, P. Sebo, R. Osicka,

. 2017 ; 9 (10) : . [pub] 20170924

Language English Country Switzerland

Document type Journal Article, Review, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc19001173

Grant support
NV16-28126A MZ0 CEP Register

Bordetellae, pathogenic to mammals, produce an immunomodulatory adenylate cyclase toxin-hemolysin (CyaA, ACT or AC-Hly) that enables them to overcome the innate immune defense of the host. CyaA subverts host phagocytic cells by an orchestrated action of its functional domains, where an extremely catalytically active adenylyl cyclase enzyme is delivered into phagocyte cytosol by a pore-forming repeat-in-toxin (RTX) cytolysin moiety. By targeting sentinel cells expressing the complement receptor 3, known as the CD11b/CD18 (αMβ₂) integrin, CyaA compromises the bactericidal functions of host phagocytes and supports infection of host airways by Bordetellae. Here, we review the state of knowledge on structural and functional aspects of CyaA toxin action, placing particular emphasis on signaling mechanisms by which the toxin-produced 3',5'-cyclic adenosine monophosphate (cAMP) subverts the physiology of phagocytic cells.

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$a Masin, Jiri $u Institute of Microbiology of the CAS, v.v.i., 142 20 Prague, Czech Republic. masin@biomed.cas.cz.
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