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β-Defensins Coordinate In Vivo to Inhibit Bacterial Infections of the Trachea

The Public Health Research Institute Center, Rutgers New Jersey Medical School, Newark, NJ 07103, USA
Division of Pulmonary and Critical Care Medicine, Department of Medicine, Rutgers New Jersey Medical School, Newark, NJ 07103, USA
Department of Oral Biology, Rutgers New Jersey Dental School, Newark, NJ 07103, USA
Author to whom correspondence should be addressed.
Present address: Division of Infectious Diseases and Global Medicine, Department of Medicine, University of Florida College of Medicine, Gainesville, FL 32610, USA.
Present address: Department of Oral Biology, University of Florida College of Dentistry, Gainesville, FL 32610, USA.
Vaccines 2018, 6(3), 57;
Received: 8 August 2018 / Revised: 21 August 2018 / Accepted: 25 August 2018 / Published: 28 August 2018
PDF [2886 KB, uploaded 28 August 2018]


β-defensins are predicted to play an important role in innate immunity against bacterial infections in the airway. We previously observed that a type III-secretion product of Bordetella bronchiseptica inhibits the NF-κB-mediated induction of a β-defensin in airway epithelial cells in vitro. To confirm this in vivo and to examine the relative roles of other β-defensins in the airway, we infected wild-type C57BL/6 mice and mice with a deletion of the mBD-1 gene with B. bronchiseptica wild-type strain, RB50 and its mutant strain lacking the type III-secretion system, WD3. The bacteria were quantified in the trachea and the nasal tissue and mRNA levels of mouse β-defensin-3 (mBD-3) were assessed after 24 h. Infection with the wild-type bacterial strain resulted in lower mBD-3 mRNA levels in the trachea than in mice infected with the type III-deficient strain. Furthermore, we observed an increase in bacterial numbers of RB50 only in the tracheas of mBD-1-deficient mice. Neutrophils were also more abundant on the trachea in RB50 infected WT mice but not in the bronchiolar lavage fluid (BAL), compared with WD3 infected WT and mBD-1−/− mice, indicating that the coordination of β-defensin chemotactic effects may be confined to tracheal epithelial cells (TEC). RB50 decreased the ability of mice to mount an early specific antibody response, seven days after infection in both WT and mBD-1−/− mice but there were no differences in titers between RB50-infected WT and mBD-1−/− mice or between WD3-infected WT and mBD-1−/− mice, indicating mBD-1 was not involved in induction of the humoral immune response to the B. bronchiseptica. Challenge of primary mouse TEC in vitro with RB50 and WD3, along with IL-1β, further corroborated the in vivo studies. The results demonstrate that at least two β-defensins can coordinate early in an infection to limit the growth of bacteria in the trachea. View Full-Text
Keywords: β-defensins; Bordetella bronchiseptica; epithelial cells; innate immunity β-defensins; Bordetella bronchiseptica; epithelial cells; innate immunity

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Ryan, L.K.; Wu, J.; Schwartz, K.; Yim, S.; Diamond, G. β-Defensins Coordinate In Vivo to Inhibit Bacterial Infections of the Trachea. Vaccines 2018, 6, 57.

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