Proteomic response of 16HBE14o- human bronchial epithelial cells to Bordetella pertussis infection.

CARLOS BAROLI; FRANK SCHMIDT; KRISTIN SURMANN; MARTINA DEBANDI; CHRISTIAN HENTSCHKER; MARIA EUGENIA RODRIGUEZ; YANINA LAMBERTI; MANUELA GESELL SALAZAR; MARIELA CARRICA; UWE VÖLKER

Congreso; LXVI Reunión Anual de la Sociedad Argentina de Inmunología (SAI).; 2018

Sociedad Argentina de Inmunología

The airway epithelium is considered central to the orchestration of pulmonary inflammation and is critically involved in the regulation of immune responses. Previous studies indicated that Bordetella pertussis (Bp) is able to enter and survive in compartments with early-endosomal characteristics in respiratory epithelial cells suggesting that this pathogen has developed strategies to exploit host functions for survival. Pertussis toxin (PT) plays a major role in modulating host responses. Here, we focused on host proteome alterations induced by Bp in epithelial cells in order to better understand this interaction. To this end, the cell line 16HBE14o- (provided by Dr. Cozens), which displays characteristic features of primary bronchial epithelial cells, was incubated with Bordetella pertussis Tohama I wild type or an isogenic mutant lacking PT for 4.5 h and 8 h at a multiplicity of infection of one. The host cell response was compared to a similarly treated uninfected control on proteome level by nanoLC-MS/MS in data independent acquisition (DIA) mode. Of the 2854 quantitatively monitored 719 proteins displayed significantly altered levels upon Bp infection compared with the control (p