Characterization of Brucella abortus S19 as a challenge strain for use in a mouse model of brucellosis

2021 ◽  
pp. 104809
Author(s):  
Jessica M. Jacob ◽  
Roy Curtiss
Keyword(s):  
Mouse Model ◽  
Brucella Abortus ◽  
Challenge Strain

scholarly journals Differential Requirements for VirB1 and VirB2 during Brucella abortus Infection

2004 ◽  
Vol 72 (9) ◽  
pp. 5143-5149 ◽  
Author(s):  
Andreas B. den Hartigh ◽  
Yao-Hui Sun ◽  
David Sondervan ◽  
Niki Heuvelmans ◽  
Marjolein O. Reinders ◽  
...  
Keyword(s):  
Mouse Model ◽  
Brucella Abortus ◽  
Persistent Infection ◽  
Host Cells ◽  
Intracellular Replication ◽  
Bacterial Surface ◽  
Type Iv

ABSTRACT The Brucella abortus virB operon, encoding a type IV secretion system (T4SS), is required for intracellular replication and persistent infection in the mouse model. The products of the first two genes of the virB operon, virB1 and virB2, are predicted to be localized at the bacterial surface, where they could potentially interact with host cells. Studies to date have focused on characterization of transposon mutations in these genes, which are expected to exert polar effects on downstream genes in the operon. In order to determine whether VirB1 and VirB2 are required for the function of the T4SS apparatus, we constructed and characterized nonpolar deletion mutations of virB1 and virB2. Both mutants were shown to be nonpolar, as demonstrated by their ability to express the downstream gene virB5 during stationary phase of growth in vitro. Both VirB1 and VirB2 were essential for intracellular replication in J774 macrophages. The nonpolar virB2 mutant was unable to cause persistent infection in the mouse model, demonstrating the essential role of VirB2 in the function of the T4SS apparatus during infection. In contrast, the nonpolar virB1 mutant persisted at wild-type levels, showing that the function of VirB1 is dispensable in the mouse model of persistent infection.

Characterization of liver GSD IX γ2 pathophysiology in a novel Phkg2−/− mouse model

2021 ◽  
Vol 132 ◽  
pp. S237
Author(s):  
Rebecca Gibson ◽  
Jeong-A Lim ◽  
Leticia Flores ◽  
Su Jin Choi ◽  
Sarah Young ◽  
...  
Keyword(s):  
Mouse Model

scholarly journals Characterization of a Mouse Model for Thrombomodulin Deficiency

2001 ◽  
Vol 21 (9) ◽  
pp. 1531-1537 ◽  
Author(s):  
Hartmut Weiler ◽  
Volkhard Lindner ◽  
Bryce Kerlin ◽  
Berend H. Isermann ◽  
Sara B. Hendrickson ◽  
...  
Keyword(s):  
Mouse Model

Metabolic Characterization of the R6/2 Transgenic Mouse Model of Huntington's Disease by High-Resolution MAS1H NMR Spectroscopy

2006 ◽  
Vol 5 (3) ◽  
pp. 483-492 ◽  
Author(s):  
Tsz M. Tsang ◽  
Ben Woodman ◽  
Gerard A. Mcloughlin ◽  
Julian L. Griffin ◽  
Sarah J. Tabrizi ◽  
...  
Keyword(s):  
Nmr Spectroscopy ◽  
High Resolution ◽  
Mouse Model ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model

scholarly journals Induced Disruption of the Iron-Regulatory Hormone Hepcidin Inhibits Acute Inflammatory Hypoferraemia

2016 ◽  
Vol 8 (5) ◽  
pp. 517-528 ◽  
Author(s):  
Andrew E. Armitage ◽  
Pei Jin Lim ◽  
Joe N. Frost ◽  
Sant-Rayn Pasricha ◽  
Elizabeth J. Soilleux ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Brucella Abortus ◽  
Serum Iron ◽  
Vibrio Vulnificus ◽  
Iron Status ◽  
Transgenic Mouse Model ◽  
Innate Immune ◽  
Serum Hepcidin

Withdrawal of iron from serum (hypoferraemia) is a conserved innate immune antimicrobial strategy that can withhold this critical nutrient from invading pathogens, impairing their growth. Hepcidin (Hamp1) is the master regulator of iron and its expression is induced by inflammation. Mice lacking Hamp1 from birth rapidly accumulate iron and are susceptible to infection by blood-dwelling siderophilic bacteria such as Vibrio vulnificus. In order to study the innate immune role of hepcidin against a background of normal iron status, we developed a transgenic mouse model of tamoxifen-sensitive conditional Hamp1 deletion (termed iHamp1-KO mice). These mice attain adulthood with an iron status indistinguishable from littermate controls. Hamp1 disruption and the consequent decline of serum hepcidin concentrations occurred within hours of a single tamoxifen dose. We found that the TLR ligands LPS and Pam3CSK4 and heat-killed Brucella abortus caused an equivalent induction of inflammation in control and iHamp1-KO mice. Pam3CSK4 and B. abortus only caused a drop in serum iron in control mice, while hypoferraemia due to LPS was evident but substantially blunted in iHamp1-KO mice. Our results characterise a powerful new model of rapidly inducible hepcidin disruption, and demonstrate the critical contribution of hepcidin to the hypoferraemia of inflammation.

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