Abstract
Bartonella henselae, the agent of cat scratch disease and the vasculoproliferative disorders bacillary angiomatosis and peliosis hepatis, contains to date two groups of described pathogenicity factors: adhesins and type IV secretion systems. Bartonella adhesin A (BadA), the Trw system and possibly filamentous hemagglutinin act as promiscous or specific adhesins, whereas the virulence locus (Vir)B/VirD4 type IV secretion system modulates a variety of host cell functions. BadA mediates bacterial adherence to endothelial cells and extracellular matrix proteins and triggers the induction of angiogenic gene programming. The VirB/VirD4 type IV secretion system is responsible for, e.g., inhibition of host cell apoptosis, bacterial persistence in erythrocytes, and endothelial sprouting. The Trw-conjugation system of Bartonella spp. mediates host-specific adherence to erythrocytes. Filamentous hemagglutinins represent additional potential pathogenicity factors which are not yet characterized. The exact molecular functions of these pathogenicity factors and their contribution to an orchestral interplay need to be analyzed to understand B. henselae pathogenicity in detail.
Highlights
Bartonella henselae is a gram-negative, zoonotic pathogen with world-wide distribution
Research with the slow growing and fastidious B. henselae is hampered by difficulties in performing molecular genetics and by the lack of suitable animal models, two essential pathogenicity factors of B. henselae have been identified and investigated in detail in recent years: (i) Bartonella adhesin A (BadA) which mediates adhesion to the extracellular matrix and mammalian host cells and (ii) the VirB/VirD4 type IV secretion system which modulates mammalian host cell functions by injecting Bartonella effector proteins (Beps) [11,12]
The B. henselae VirB/VirD4 type IV secretion system (i) mediates rearrangements of the actin cytoskeleton resulting in the formation of bacterial aggregates on the cell surface that are subsequently internalized ("invasome” structure), (ii) triggers a proinflammatory phenotype via activation of nuclear factor (NF)-B that in turn induces the secretion of interleukin-8 and the expression of the cell adhesion molecules intercellular adhesion molecule (ICAM)-1 and E-selectin and (iii) is crucial for the inhibition of endothelial apoptosis [27]
Summary
Bartonella henselae is a gram-negative, zoonotic pathogen with world-wide distribution. Research with the slow growing and fastidious B. henselae is hampered by difficulties in performing molecular genetics and by the lack of suitable animal models, two essential pathogenicity factors of B. henselae have been identified and investigated in detail in recent years: (i) Bartonella adhesin A (BadA) which mediates adhesion to the extracellular matrix and mammalian host cells and (ii) the VirB/VirD4 type IV secretion system which modulates mammalian host cell functions by injecting Bartonella effector proteins (Beps) [11,12].
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