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. Copyright 2019 by the authors. Licensee MDPI, Basel, Switzerland.Sponsors
This research was funded by National Institutes of Health, grant numbers AI101055, AI119566, AI117095, AI135465, AI137778, AI141372 (to NC) and AI140035 (to CS).Keyword
Bacterial infectionCough
Immunomodulation
Inflammation
Leukocytosis
Pertussis toxin
Pulmonary hypertension
Respiratory disease
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https://www.scopus.com/inward/record.uri?eid=2-s2.0-85068726610&doi=10.3390%2ftoxins11070373&partnerID=40&md5=84c94709b84b1f744460f5b7b04a602f; http://hdl.handle.net/10713/10230ae974a485f413a2113503eed53cd6c53
10.3390/toxins11070373