Constitutive and Inducible Green Fluorescent Protein Expression in<i>Bartonella henselae</i>

Lee, Anthea K.; Falkow, Stanley

doi:10.1128/iai.66.8.3964-3967.1998

Cited by 41 publications

(12 citation statements)

References 20 publications

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“…The clinical UTI isolate E. coli CI5 strain [ 77 , 78 ] was kindly provided by Prof. Soman N Abraham (Duke and Duke-NUS) and was used throughout the in vitro study. The prototypic cystitis strain UTI89 [ 52 ] transformed with plasmid pANT4 expressing GFP [ 79 ] (referred to as strain SLC-295) was used for in vivo infection experiments in mice. The K12/mCherry strain (SLC-720) is E. coli K12 substr.…”

Section: Methodsmentioning

confidence: 99%

“…MG1655 transformed with an mCherry expression vector (pSLC-229). pSLC-229 was generated by replacing the GFP gene in plasmid pANT4 [ 79 ] with mCherry amplified from pXJ40_2 (a kind gift from Sohail Ahmed). Briefly, mCherry was amplified using PCR (using the primers 5’-GACTCTGAATTCATGGTGAGCAAGGGCGAGGA and 5’-GATCCTGCATGCTTACTTGTACAGCTCGTCCATGC).…”

Section: Methodsmentioning

confidence: 99%

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Intracellular Uropathogenic E. coli Exploits Host Rab35 for Iron Acquisition and Survival within Urinary Bladder Cells

et al. 2015

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Recurrent urinary tract infections (UTIs) caused by uropathogenic E. coli (UPEC) are common and morbid infections with limited therapeutic options. Previous studies have demonstrated that persistent intracellular infection of bladder epithelial cells (BEC) by UPEC contributes to recurrent UTI in mouse models of infection. However, the mechanisms employed by UPEC to survive within BEC are incompletely understood. In this study we aimed to understand the role of host vesicular trafficking proteins in the intracellular survival of UPEC. Using a cell culture model of intracellular UPEC infection, we found that the small GTPase Rab35 facilitates UPEC survival in UPEC-containing vacuoles (UCV) within BEC. Rab35 plays a role in endosomal recycling of transferrin receptor (TfR), the key protein responsible for transferrin–mediated cellular iron uptake. UPEC enhance the expression of both Rab35 and TfR and recruit these proteins to the UCV, thereby supplying UPEC with the essential nutrient iron. Accordingly, Rab35 or TfR depleted cells showed significantly lower intracellular iron levels and reduced ability to support UPEC survival. In the absence of Rab35, UPEC are preferentially trafficked to degradative lysosomes and killed. Furthermore, in an in vivo murine model of persistent intracellular infection, Rab35 also colocalizes with intracellular UPEC. We propose a model in which UPEC subverts two different vesicular trafficking pathways (endosomal recycling and degradative lysosomal fusion) by modulating Rab35, thereby simultaneously enhancing iron acquisition and avoiding lysosomal degradation of the UCV within bladder epithelial cells. Our findings reveal a novel survival mechanism of intracellular UPEC and suggest a potential avenue for therapeutic intervention against recurrent UTI.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Intracellular Uropathogenic E. coli Exploits Host Rab35 for Iron Acquisition and Survival within Urinary Bladder Cells

et al. 2015

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“…Bacterial strains were K. pneumoniae laboratory strain and Kp52145 from the Collection of Institute Pasteur in Paris, S. typhimurium (ATCC 14028), P. aeruginosa strains PT5 and PT531 (Cosson et al ., 2002), E. coli strains DH5α (Invitrogen), uropathogenic N2173‐96 (Centre national des bactéries entéropathogènes, Bern, Switzerland) and B/r (Gerisch, 1959), B. subtilis strain 36.1 (Ratner and Newell, 1978), S. aureus RN6390, E. faecalis (ATCC 29212) and L. monocytogenes L028. A K. pneumoniae strain expressing GFP was obtained by introducing the GFP‐expressing plasmid pANT5 (Lee and Falkow, 1998) into our laboratory strain.…”

Section: Methodsmentioning

confidence: 99%

Specific host genes required for the killing of Klebsiella bacteria by phagocytes

Benghezal¹,

Fauvarque²,

Tournebize³

et al. 2006

Cell Microbiol

127

137

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SummaryThe amoeba Dictyostelium discoideum shares many traits with mammalian macrophages, in particular the ability to phagocytose and kill bacteria. In response, pathogenic bacteria use conserved mechanisms to fight amoebae and mammalian phagocytes. Here we developed an assay using Dictyostelium to monitor phagocyte-bacteria interactions. Genetic analysis revealed that the virulence of Klebsiella pneumoniae measured by this test is very similar to that observed in a mouse pneumonia model. Using this assay, two new host resistance genes ( PHG1 and KIL1 ) were identified and shown to be involved in intracellular killing of K. pneumoniae by phagocytes. Phg1 is a member of the 9TM family of proteins, and Kil1 is a sulphotransferase. The loss of PHG1 resulted in Dictyostelium susceptibility to a small subset of bacterial species including K. pneumoniae . Remarkably, Drosophila mutants deficient for PHG1 also exhibited a specific susceptibility to K. pneumoniae infections. Systematic analysis of several additional Dictyostelium mutants created a two-dimensional virulence array, where the complex interactions between host and bacteria are visualized.

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“…The wild-type strain (B. quintana JK31, deposited at www.BEIresources.org #NR-31832; Zhang et al, 2004) and the GFPexpressing isogenic strain of B. quintana JK31 (Lee & Falkow, 1998;Park et al, 2001) were maintained in a Biosafety Level 2 facility. B. quintana from frozen stocks was cultured on chocolate agar plates in candle extinction jars at 378C for 10 days and then passed to fresh plates for an additional 5-7 days of growth prior to use (Zhang et al, 2004).…”

Section: B Quintana Culturementioning

confidence: 99%

Comparison of the proliferation and excretion of Bartonella quintana between body and head lice following oral challenge

Kim

Previte

Yoon

et al. 2017

Insect Molecular Biology

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Human body and head lice are highly related hematophagous ectoparasites but only the body louse has been shown to transmit Bartonella quintana, the causative agent of trench fever. The mechanisms by which body lice became a vector for B. quintana, however, are poorly understood. Following the oral challenge, green fluorescence protein-expressing B. quintana proliferated over 9 days post-challenge with the number of bacteria being significantly higher in whole body versus head lice. The numbers of B. quintana detected in feces from infected lice, however, were approximately the same in both lice. Nevertheless, the viability of B. quintana, was significantly higher in body louse feces. Comparison of immune responses in alimentary tract tissues revealed that basal transcription levels of peptidoglycan recognition protein and defensins were lower in body lice and the transcription of defensin 1 was up-regulated by oral challenge with wild-type B. quintana in head but not in body lice. In addition, the level of cytotoxic reactive oxygen species generated by epithelial cells was significantly lower in body lice. Although speculative at this time, the reduced immune response is consistent with the higher vector competence seen in body versus head lice in terms of B. quintana infection.

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Constitutive and Inducible Green Fluorescent Protein Expression inBartonella henselae

Cited by 41 publications

References 20 publications

Intracellular Uropathogenic E. coli Exploits Host Rab35 for Iron Acquisition and Survival within Urinary Bladder Cells

Intracellular Uropathogenic E. coli Exploits Host Rab35 for Iron Acquisition and Survival within Urinary Bladder Cells

Specific host genes required for the killing of Klebsiella bacteria by phagocytes

Comparison of the proliferation and excretion of Bartonella quintana between body and head lice following oral challenge

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