Pertussis toxin exacerbates and prolongs airway inflammatory responses during Bordetella pertussis infection.
Ontology highlight
ABSTRACT: Throughout infection, pathogenic bacteria induce dramatic changes in host transcriptional repertoires. An understanding of how bacterial factors influence host reprogramming will provide insight into disease pathogenesis. In the human respiratory pathogen Bordetella pertussis, the causative agent of whooping cough, pertussis toxin (PT) is a key virulence factor that promotes colonization, suppresses innate immune responses during early infection, and causes systemic disease symptoms. To determine the full extent of PT-associated gene regulation in the airways through the peak of infection, we measured global transcriptional profiles in the lungs of BALB/c mice infected with wild-type (WT) or PT-deficient (ΔPT) B. pertussis. ΔPT bacteria were inoculated at a dose equivalent to the WT dose a
SUBMITTER: Connelly CE
PROVIDER: S-EPMC3497438 | biostudies-literature | 2012 Dec
REPOSITORIES: biostudies-literature
ACCESS DATA