Figure 4.

Haemophilus influenzae autotransporter proteins. (A) Summary of key features of H. influenzae autotransporter proteins. (B) Schematic of the role of H. influenzae autotransporter proteins in the pathogenesis of disease. (a) Hap and Hia facilitate H. influenzae attachment to epithelial cells. Hap also promotes adherence to the ECM on the cell layer and at areas of damaged epithelium (*). Hap autoproteolysis is inhibited by SLPI, resulting in the retention of Hap_s on the bacterial surface. IgA1 protease is released from the bacterial surface and cleaves human IgA1. (b) Once bacteria have adhered, Hap–Hap interactions lead to microcolony formation. (c) Microcolony formation leads to the establishment of a biofilm that is resistant to host immune factors. (d) In the absence of SLPI, Hap autoproteolytic activity allows some bacteria to disperse, presumably to new sites of infection. (e) Hap-mediated attachment promotes bacterial invasion into epithelial cells, potentially providing a protected niche, and allowing bacterial evasion of local immune mechanisms.