Journal
TOXINS
Volume 9, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/toxins9100300
Keywords
adenylate cyclase toxin; Bordetella; (2) integrins; cAMP; CD11b; CD18; cell signaling; complement receptor 3; innate immunity; membrane pores; repeats-in-toxin
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Funding
- Grant Agency of the Czech Republic [GA15-09157S, 16-05919S]
- Ministry of Education, Youth and Sports of the Czech Republic [LM2015064]
- Charles University in Prague [UNCE204025/2012]
- Grant Agency of the Charles University in Prague [228216]
- Ministry of Health of the Czech Republic [NV16-28126A]
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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 ((M2)) 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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