Infection of respiratory epithelial cells by NTHi375 mutant strains lacking the <i>ompP5</i> and <i>hap</i> genes.

<p>Bacterial adhesion is shown in the left and invasion in the right panels, in all sections of this figure. <b>(A)</b> NTHi375 interplay with upper and lower human epithelial airways. NTHi375 adhesion to- and invasion of nasal RPMI 2650, pharynx Detroit 562 and bronchial H-292 epithelia and type II pneumocytes A549. Effect of <i>ompP5</i> and <i>hap</i> gene disruption on NTHi interplay with RPMI 2650 nasal <b>(B)</b>, Detroit 562 pharynx <b>(C)</b>, NCI H-292 bronchial <b>(D)</b>, and A549 type II alveolar <b>(E)</b> epithelial cells. NTHi375, Δ<i>ompP5</i>, Δ<i>hap</i> and Δ<i>ompP5</i>Δ<i>hap</i> strains were used to assess bacterial adhesion and invasion. <b>(F)</b> Effect of <i>ompP5</i> gene disruption on Hi RdKW20 interplay with NCI H-292 bronchial and A549 type II alveolar epithelial cells. Hi RdKW20 and Δ<i>ompP5</i> mutant strains were used to assess bacterial adhesion and invasion. Experiments were performed in triplicate in at least three independent occasions (n≥9).