Mediates bacterial adherence to host endothelial cells and host extracellular matrix proteins (collagen type I, III, IV, laminin and fibronectin). Static versus dynamic adherence results differ slightly; in dynamic adherence studies bacteria bind to fixed components under a constant defined flow rate to simulate in vivo infection conditions (PubMed:15534369, PubMed:17060468, PubMed:18627378, PubMed:21536788, PubMed:23163798). Induces secretion of host proangiogenic cytokines such as VEGFA, ADM, IGFBP-3 and IL-8. May prevent bacterial phagocytosis by macrophages (PubMed:15534369) (Probable). Probably mediates bacterial autoagglutination (PubMed:17060468, PubMed:18627378). Negatively impacts type IV secretion system effectors (VirB/D4 T4SS and its substrate Bep proteins), possibly by preventing close association of host and bacterial cells. This implies the 2 factors are expressed at different times during infection (Probable). Homotrimer (Probable). Crystals of the head region form trimers (PubMed:18688279). Forms long (about 240 nm) filaments extending from the cell surface, which were initially called type IV pili (PubMed:15534369, PubMed:18627378, PubMed:21536788, PubMed:21981119, PubMed:23163798). The C-terminal translocator domain is localized in the outer membrane and the passenger domain is at the cell surface (By similarity). The N-terminus (residues 48-376) performs most of the host-associated functions of the protein and binds collagen. The large central domain (composed of neck-stalk repeats about residue 470-2850) is required to bind host fibronectin and contributes to host cell adherence, collagen-binding and induction of host proangiogenic factors. The signal peptide, cleaved at the inner membrane, guides the autotransporter protein to the periplasmic space. Then, insertion of the C-terminal translocator domain in the outer membrane forms a hydrophilic pore for the translocation of the passenger domain to the bacterial cell surface. No longer binds to host cells or host extracellular matrix proteins, loss of bacterial 'type IV-like pili'. Bacteria are more frequently phagocytosed by murine J774 macrophages. Infected HeLa cells no longer secrete proangiogenic factors such as VEGFA, ADM, IGFBP3 or IL-8 (PubMed:15534369). Decreased binding to host epithelial cells and to host extracellular matrix components vitronectin, hyaluronate, fibronectin, laminin, collagens I, III and IV under static and dynamic flow conditions (PubMed:21536788). Antisera to this protein are frequently present in humans and animals infected by B.henselae, suggesting it might be useful as a marker for B.henselae infection. Infection with B.henselae leads to cat scratch disease in immunocompetent individuals and bacillary angiomatosis, tumorous proliferations of endothelial cells in the skin and internal organs in immunocompromised patients. Belongs to the autotransporter-2 (AT-2) (TC 1.B.40) family.