The Trw type IV secretion system of Bartonella mediates host-specific
adhesion,to erythrocytes.
PLoS Pathog. 2010 Jun 10;6(6):e1000946.
The Trw type IV secretion system of Bartonella mediates
host-specific adhesion to erythrocytes.
Vayssier-Taussat M, Le Rhun D, Deng HK, Biville F, Cescau S,
Danchin A, Marignac G, Lenaour E, Boulouis HJ, Mavris M, Arnaud
L, Yang H, Wang J, Quebatte M, Engel P, Saenz H, Dehio C.
Unite Sous Contrat Bartonella, INRA, Maisons-Alfort, France.
mvayssier@vet-alfort.fr
Bacterial pathogens typically infect only a limited range of
hosts; however, the genetic mechanisms governing host-specificity
are poorly understood. The alpha-proteobacterial genus Bartonella
comprises 21 species that cause host-specific intraerythrocytic
bacteremia as hallmark of infection in their respective mammalian
reservoirs, including the human-specific pathogens Bartonella
quintana and Bartonella bacilliformis that cause trench fever and
Oroya fever, respectively. Here, we have identified bacterial
factors that mediate host-specific erythrocyte colonization in
the mammalian reservoirs.
Using mouse-specific Bartonella birtlesii, human-specific
Bartonella quintana, cat-specific Bartonella henselae and
rat-specific Bartonella tribocorum, we established in vitro
adhesion and invasion assays with isolated erythrocytes that
fully reproduce the host-specificity of erythrocyte infection as
observed in vivo. By signature-tagged mutagenesis of B. birtlesii
and mutant selection in a mouse infection model we identified
mutants impaired in establishing intraerythrocytic bacteremia.
Among 45 abacteremic mutants, five failed to adhere to and invade
mouse erythrocytes in vitro. The corresponding genes encode
components of the type IV secretion system (T4SS) Trw,
demonstrating that this virulence factor laterally acquired by
the Bartonella lineage is directly involved in adherence to
erythrocytes. Strikingly, ectopic expression of Trw of
rat-specific B. tribocorum in cat-specific B. henselae or
human-specific B.
quintana expanded their host range for erythrocyte infection to
rat, demonstrating that Trw mediates host-specific erythrocyte
infection. A molecular evolutionary analysis of the trw locus
further indicated that the variable, surface-located TrwL and
TrwJ might represent the T4SS components that determine
host-specificity of erythrocyte parasitism. In conclusion, we
show that the laterally acquired Trw T4SS diversified in the
Bartonella lineage to facilitate host-restricted adhesion to
erythrocytes in a wide range of mammals.
Publication Types:
Research Support, Non-U.S. Gov't
http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pu
bmed&id=20548954&retmode=ref&cmd=prlinks
PMID: 20548954 [PubMed - in process]
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