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Abstract
Pertussis, caused by respiratory tract infection with the bacterial pathogen Bordetella pertussis, has long been considered to be a toxin-mediated disease. Bacteria adhere and multiply extracellularly in the airways and release several toxins, which have a variety of effects on the host, both local and systemic. Predominant among these toxins is pertussis toxin (PT), a multi-subunit protein toxin that inhibits signaling through a subset of G protein-coupled receptors in mammalian cells. PT activity has been linked with severe and lethal pertussis disease in young infants and a detoxified version of PT is a common component of all licensed acellular pertussis vaccines. The role of PT in typical pertussis disease in other individuals is less clear, but significant evidence supporting its contribution to pathogenesis has been accumulated from animal model studies. In this review we discuss the evidence indicating a role for PT in pertussis disease, focusing on its contribution to severe pertussis in infants, modulation of immune and inflammatory responses to infection, and the characteristic paroxysmal cough of pertussis.
Highlights
Pertussis toxin (PT) is an important virulence factor of the respiratory pathogenBordetella pertussis [1]
We have found that PT activity is associated with prolonged and exacerbated respiratory inflammatory pathology in mouse models of B. pertussis infection [93,108]
Leukocytosis and pulmonary hypertension are associated with PT-mediated dysfunction in organs outside the airways, suggesting that, in infants, either B. pertussis itself or its toxins are capable of disseminating beyond the primary site of infection
Summary
Pertussis toxin (PT) is an important virulence factor of the respiratory pathogen. PT is an adenosine diphosphate (ADP)-ribosylating protein toxin that inhibits signaling through a subset of G protein-coupled receptors (GPCRs) in mammalian cells. Pertussis has long been considered a toxin-mediated disease, with PT promoting the majority of pathogenic manifestations [2]. Evidence from both human disease and animal models of B. pertussis infection strongly indicates that PT is a major contributor to severe pertussis disease. We consider the association of PT activity with three different (but possibly related) aspects of pertussis disease: Severe disease in young infants; immune and inflammatory responses; and paroxysmal cough
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