Figure 2.

A. baumannii-host cell interactions. Extracellular A. baumannii experiences a metal-limited environment at least in part due to metal-binding host proteins and intracellular localization of metals, e.g., red blood cells (RBCs). A. baumannii attaches to host cells through interactions between fibronectin and bacterial outer membrane proteins (OMPs), such as OmpA, as well as Type IV collagen via Ata. These OMPs may bind to other host cell proteins, for example the interaction of OMP ChoP with platelet activating factor receptor (PFAR). Fimbriae also contribute to eukaryotic cell adherence. Invasion into epithelial cells occurs via host cell actin filament and microtubule reorganization, recruitment of β-arrestin and clathrin, and a bacterial uptake via a zipper-like mechanism. Although A. baumannii can persist intracellularly and includes entry into endosomes, the intracellular trafficking of A. baumannii is not clear. Eukaryotic cell proteins NRAMP1, ZIP8, ZnTs, and other transporters pump essential metals out of endocytic vesicles and the cytoplasm, limiting the intracellular pool available to pathogens. The physiological relevance of the intracellular lifecycle of A. baumannii remains to be understood. One consequence of host cell exposure to A. baumannii is apoptosis. It is possible that cell death and/or host cell invasion serve to permit A. baumannii dissemination to deeper tissues leading to invasive disease.