Pertussis, caused by Bordetella pertussis (B. pertussis), is reemerging worldwide due to vaccine inefficacy. The hallmarks of infection are extreme lymphocytosis and delayed recovery, which are partially associated with pertussis toxin. Lymphocytes migrate to infected tissues using trafficking receptors. Specific combinations of these lymphocyte trafficking receptors are identified for skin and gut but are not well established for lung.
This study focused on the effect of pertussis toxin on lung-associated trafficking receptors and tested the hypothesis that pertussis toxin alters dendritic cell imprinting of lung trafficking receptors on T cells, thus delaying resolution of the infection. B. pertussis-infected mice were compared with pertussis toxin-deficient strains. Imprinting of trafficking receptors on allogeneic T cells by dendritic cells derived from Bordetella-infected mice was analyzed by flow cytometry.
Mice infected with Bordetella strains showed an increase in mature dendritic cells on day 5 post-infection. Despite their mature phenotype, dendritic cells from B. pertussis infection, were compromised in their ability to imprint lung trafficking receptors on allogenic T cells. These results indicated a pertussis toxin-dependent defect in dendritic cell imprinting of lung trafficking receptors on T cells. In conclusion, this study provides important data for future vaccine development against respiratory pathogens
