Zebrafish Embryo Model of<i>Bartonella henselae</i>Infection

Lima, Amorce; Byeong, J.; Amin, Jahanshah; Smith, Lisa K.; Anderson, Burt

doi:10.1089/zeb.2014.1001

Cited by 14 publications

(12 citation statements)

References 72 publications

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“…For experiments using strains harboring pNS2‐derived plasmids, the culture medium was supplemented with 50 μg/ml kanamycin (Gillaspie et al., ). The construction of a nonpolar in‐frame deletion mutant of badA (BH01510) has been previously described (Lima, Cha, Amin, Smith, & Anderson, ). The ∆ badA mutant served as a control for experiments examining badA expression and biofilm formation.…”

Section: Methodsmentioning

confidence: 99%

A family of genus‐specific RNAs in tandem with DNA‐binding proteins control expression of the badA major virulence factor gene in Bartonella henselae

Carroll

Weiss

et al. 2016

MicrobiologyOpen

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Bartonella henselae is a gram‐negative zoonotic bacterium that causes infections in humans including endocarditis and bacillary angiomatosis. B. henselae has been shown to grow as large aggregates and form biofilms in vitro. The aggregative growth and the angiogenic host response requires the trimeric autotransporter adhesin BadA. We examined the transcriptome of the Houston‐1 strain of B. henselae using RNA‐seq revealing nine novel, highly‐expressed intergenic transcripts (Bartonella regulatory transcript, Brt1‐9). The Brt family of RNAs is unique to the genus Bartonella and ranges from 194 to 203 nucleotides with high homology and stable predicted secondary structures. Immediately downstream of each of the nine RNA genes is a helix‐turn‐helix DNA‐binding protein (transcriptional regulatory protein, Trp1‐9) that is poorly transcribed under the growth conditions used for RNA‐seq. Using knockdown or overexpressing strains, we show a role of both the Brt1 and Trp1 in the regulation of badA and also in biofilm formation. Based on these data, we hypothesize that Brt1 is a trans‐acting sRNA that also serves as a cis‐acting riboswitch to control the expression of badA. This family of RNAs together with the downstream Trp DNA‐binding proteins represents a novel coordinated regulatory circuit controlling expression of virulence‐associated genes in the bartonellae.

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Section: Methodsmentioning

confidence: 99%

A family of genus‐specific RNAs in tandem with DNA‐binding proteins control expression of the badA major virulence factor gene in Bartonella henselae

Carroll

Weiss

et al. 2016

MicrobiologyOpen

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“…BadA prevents bacteria from being phagocytized and also stimulates endothelial cell proliferation by inducing a proangiogenic host cell response through activation of Hif-1, a crucial transcription factor for angiogenic cytokine secretion (77,323,324). A ΔbadA mutant of B. henselae was shown to exhibit reduced replication and a weakened proangiogenic host response in a zebrafish embryo model (325).…”

Section: Virulence Factorsmentioning

confidence: 99%

“…Surface localization of BadA can be seen in both the Houston-1 and Marseille strains but not the isogenic badA deletion mutants (Houston-1 ΔbadA mutant [C] and Marseille ΔbadA mutant [D]). The markerless, nonpolar in-frame Houston-1 deletion mutant was constructed as previously described (325). The Marseille deletion mutant was constructed by the same approach (unpublished data).…”

Section: Virulence Factorsmentioning

confidence: 99%

Bartonella Species, an Emerging Cause of Blood-Culture-Negative Endocarditis

et al. 2017

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Since the reclassification of the genus in 1993, the number of species has grown from 1 to 45 currently designated members. Likewise, the association of different species with human disease continues to grow, as does the range of clinical presentations associated with these bacteria. Among these, blood-culture-negative endocarditis stands out as a common, often undiagnosed, clinical presentation of infection with several different species. The limitations of laboratory tests resulting in this underdiagnosis of endocarditis are discussed. The varied clinical picture of infection and a review of clinical aspects of endocarditis caused by are presented. We also summarize the current knowledge of the molecular basis of pathogenesis, focusing on surface adhesins in the two species that most commonly cause endocarditis, and. We discuss evidence that surface adhesins are important factors for autoaggregation and biofilm formation by species. Finally, we propose that biofilm formation is a critical step in the formation of vegetative masses during-mediated endocarditis and represents a potential reservoir for persistence by these bacteria.

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“…Using Bh Houston-1, Bh Houston-1 ∆badA (a complete in-frame badA deletion mutant) 24 and Bh Houston-1 ∆badA /pNS2P Trc badA ( a partial complement of badA consisting of the N-terminal head, a truncated neck region with only the terminal neck domain, and the C-terminal membrane anchor) (this study), we investigated the differences in gene expression, biofilm formation and composition. The size of BadA varies between different strains of the Bh owing to its stalk region size.…”

Section: Discussionmentioning

confidence: 99%

The trimeric autotransporter adhesin BadA is required for in vitro biofilm formation by Bartonella henselae

Okaro

Green

Mohapatra

et al. 2019

npj Biofilms Microbiomes

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Bartonella henselae (Bh) is a Gram-negative rod transmitted to humans by a scratch from the common house cat. Infection of humans with Bh can result in a range of clinical diseases including lymphadenopathy observed in cat-scratch disease and more serious disease from persistent bacteremia. It is a common cause of blood-culture negative endocarditis as the bacterium is capable of growing as aggregates, and forming biofilms on infected native and prosthetic heart valves. The aggregative growth requires a trimeric autotransporter adhesin (TAA) called Bartonella adhesin A (BadA). TAAs are found in all Bartonella species and many other Gram-negative bacteria. Using Bh Houston-1, Bh Houston-1 ∆badA and Bh Houston-1 ∆badA/pNS2PTrcbadA (a partial complement of badA coding for a truncated protein of 741 amino acid residues), we analyze the role of BadA in adhesion and biofilm formation. We also investigate the role of environmental factors such as temperature on badA expression and biofilm formation. Real-time cell adhesion monitoring and electron microscopy show that Bh Houston-1 adheres and forms biofilm more efficiently than the Bh Houston-1 ∆badA. Deletion of the badA gene significantly decreases adhesion, the first step in biofilm formation in vitro, which is partially restored in Bh Houston-1 ∆badA/pNS2PTrcbadA. The biofilm formed by Bh Houston-1 includes polysaccharides, proteins, and DNA components and is susceptible to enzymatic degradation of these components. Furthermore, both pH and temperature influence both badA expression and biofilm formation. We conclude that BadA is required for optimal adhesion, agglutination and biofilm formation.

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Zebrafish Embryo Model ofBartonella henselaeInfection

Cited by 14 publications

References 72 publications

A family of genus‐specific RNAs in tandem with DNA‐binding proteins control expression of the badA major virulence factor gene in Bartonella henselae

A family of genus‐specific RNAs in tandem with DNA‐binding proteins control expression of the badA major virulence factor gene in Bartonella henselae

Bartonella Species, an Emerging Cause of Blood-Culture-Negative Endocarditis

The trimeric autotransporter adhesin BadA is required for in vitro biofilm formation by Bartonella henselae

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