Cholesterol-dependent attachment of human respiratory cells by<i>Bordetella pertussis</i>

Lamberti, Yanina Andrea; Hayes, Jimena Álvarez; Vidakovics, María Laura Anabella Pérez; Rodrı́guez, Marı́a Eugenia

doi:10.1111/j.1574-695x.2009.00557.x

Cited by 15 publications

(18 citation statements)

References 28 publications

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“…Exocytosis of the lysosomal enzyme β-glucuronidase was determined as previously described [38], with minor modifications. Briefly, 2x10 5 neutrophils were incubated with bacteria at a multiplicity of infection (MOI) of 300 for 10 min at 37°C and centrifuged at 300 x g. Supernatants were further centrifuged at 10,000 x g for 10 min to eliminate bacteria.…”

Section: Methodsmentioning

confidence: 99%

Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms

et al. 2017

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B. parapertussis is a whooping cough etiological agent with the ability to evade the immune response induced by pertussis vaccines. We previously demonstrated that in the absence of opsonic antibodies B. parapertussis hampers phagocytosis by neutrophils and macrophages and, when phagocytosed, blocks intracellular killing by interfering with phagolysosomal fusion. But neutrophils can kill and/or immobilize extracellular bacteria through non-phagocytic mechanisms such as degranulation and neutrophil extracellular traps (NETs). In this study we demonstrated that B. parapertussis also has the ability to circumvent these two neutrophil extracellular bactericidal activities. The lack of neutrophil degranulation was found dependent on the O antigen that targets the bacteria to cell lipid rafts, eventually avoiding the fusion of nascent phagosomes with specific and azurophilic granules. IgG opsonization overcame this inhibition of neutrophil degranulation. We further observed that B. parapertussis did not induce NETs release in resting neutrophils and inhibited NETs formation in response to phorbol myristate acetate (PMA) stimulation by a mechanism dependent on adenylate cyclase toxin (CyaA)-mediated inhibition of reactive oxygen species (ROS) generation. Thus, B. parapertussis modulates neutrophil bactericidal activity through two different mechanisms, one related to the lack of proper NETs-inducer stimuli and the other one related to an active inhibitory mechanism. Together with previous results these data suggest that B. parapertussis has the ability to subvert the main neutrophil bactericidal functions, inhibiting efficient clearance in non-immune hosts.

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Section: Methodsmentioning

confidence: 99%

Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms

et al. 2017

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“…The drugs (purchased from Sigma) were maintained throughout the experiment. In separate experiments, cells were pretreated with 10 mM methyl‐ß‐cyclodextrin (MßCD; Sigma) plus 5 μg mL −1 of lovastatin (Sigma) for 15 min at 37 °C as described previously (Lamberti et al ., ) before infection with B. pertussis . In these experiments, lovastatin (5 μg mL −1 ) was maintained throughout the infection period.…”

Section: Methodsmentioning

confidence: 99%

Bordetella pertussisentry into respiratory epithelial cells and intracellular survival

et al. 2013

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Bordetella pertussis is the causative agent of pertussis, aka whooping cough. Although generally considered an extracellular pathogen, this bacterium has been found inside respiratory epithelial cells, which might represent a survival strategy inside the host. Relatively little is known, however, about the mechanism of internalization and the fate of B. pertussis inside the epithelia. We show here that B. pertussis is able to enter those cells by a mechanism dependent on microtubule assembly, lipid raft integrity, and the activation of a tyrosine-kinase-mediated signaling. Once inside the cell, a significant proportion of the intracellular bacteria evade phagolysosomal fusion and remain viable in nonacidic lysosome-associated membrane-protein-1-negative compartments. In addition, intracellular B. pertussis was found able to repopulate the extracellular environment after complete elimination of the extracellular bacteria with polymyxin B. Taken together, these data suggest that B. pertussis is able to survive within respiratory epithelial cells and by this means potentially contribute to host immune system evasion.

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“…It is a 220-kDa secreted protein encoded by fhaB that is capable of interacting with various cell types [6] through its multiple binding domains. FHA-mediated adherence of B. pertussis to the respiratory epithelium is in addition enhanced by AC-Hly [44] and the presence of cholesterol containing lipid rafts [45]. FHA might also possess immunomodulatory activities by acting on macrophages, dendritic cells and inflammation [46].…”

Section: The B Pertussis Los Endotoxinmentioning

confidence: 99%

Bordetella pertussisand pertactin-deficient clinical isolates: lessons for pertussis vaccines

Hégerlé

Guiso²

2014

Expert Review of Vaccines

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Bordetella pertussis causes whooping cough in humans, a highly transmissible respiratory disease life threatening for unvaccinated infants. Vaccination strategies were thus introduced worldwide with great success in developed countries reaching high vaccine coverage with efficacious vaccines. In the late 20th/early 21st century, acellular pertussis vaccines replaced whole cell pertussis vaccines but B. pertussis still circulates and evolves in humans, its only known reservoir. The latest transformation of this pathogen, and of its close relative Bordetella parapertussis, is the loss of pertactin production, a virulence factor included in different acellular pertussis vaccines. The real impact of this evolution on acellular pertussis vaccines efficacy and effectiveness should be assessed through standardized surveillance and isolation of B. pertussis and B. parapertussis worldwide.

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Cholesterol-dependent attachment of human respiratory cells byBordetella pertussis

Cited by 15 publications

References 28 publications

Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms

Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms

Bordetella pertussisentry into respiratory epithelial cells and intracellular survival

Bordetella pertussisand pertactin-deficient clinical isolates: lessons for pertussis vaccines

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