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Adaptive responses of human monocytes infected by Bordetella pertussis : The role of adenylate cyclase hemolysin
Author(s) -
Njamkepo Elisabeth,
Pinot Françoise,
François Dominique,
Guiso Nicole,
Polla Barbara S.,
Bachelet Maria
Publication year - 2000
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(200004)183:1<91::aid-jcp11>3.0.co;2-s
Subject(s) - bordetella pertussis , adenylate cyclase toxin , adenylate kinase , pertussis toxin , cyclase , microbiology and biotechnology , cyclic adenosine monophosphate , biology , hemolysin , g protein , signal transduction , biochemistry , receptor , bacteria , virulence , gene , genetics
The activation/adaptive responses of human monocytes exposed to Bordetella pertussis parental or mutant strains were evaluated and correlated to the expression of two bacterial toxins: adenylate cyclase‐hemolysin and pertussis toxin. The marked rise in intracellular cyclic adenosine monophosphate (cAMP) observed in monocytes infected by B. pertussis parental strain, inversely correlated with (1) the production of tumor necrosis factor α; (2) the release of superoxide anion; and (3) the expression of the 72‐kDa heat shock/stress protein, Hsp70. Experiments performed with mutants deficient in adenylate cyclase‐hemolysin or with purified bacterial toxins confirmed the key role of adenylate cyclase‐hemolysin in the control of monocytes' response to infection by B. pertussis. This bacterial strategy primarily involves evasion from antimicrobial defenses and, eventually, the sacrifice of the host cell. J. Cell. Physiol. 183:91–99, 2000. © 2000 Wiley‐Liss, Inc.