BBB07 contributes to, but is not essential for, Borrelia burgdorferi infection in mice

Hahn, Beth L.; Anderson, Phillip N.; Lu, Zouyan; Danner, Rebecca; Zhou, Zhipeng; Hyun, Noorie; Gao, Lihui; Lin, Tao; Norris, Steven J.; Coburn, Jenifer

doi:10.1099/mic.0.000972

Cited by 2 publications

(1 citation statement)

References 15 publications

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“…Pathogens often express the RGD motif and use it as a virulence factor as it allows them to attach to and subsequently infect host cells. Examples of pathogens that use an RGD-containing protein to mediate adhesion to host cells include Bordetella pertussis (filamentous hemagglutinin) ( 79 ), Streptococcus agalactiae ( scpB ) ( 53 ), Mycobacterium tuberculosis (Peptidyl Prolyl Isomerase A) ( 58 ), Borrelia burgdorferi (BBB07) ( 59 ), Helicobacter pylori (CagL) ( 80 ). Candida albicans (Sap6) ( 81 ), SARS-CoV-2 ( 82 ), Coxsackievirus A9 (VP1) ( 83 ) and HIV-1 (Tat protein) ( 70 ) also express RGD-containing proteins.…”

Section: Pathogen Interaction With Platelet Haemostasis Receptorsmentioning

confidence: 99%

Sepsis – it is all about the platelets

Cox

2023

Front. Immunol.

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Sepsis is accompanied by thrombocytopenia and the severity of the thrombocytopenia is associated with mortality. This thrombocytopenia is characteristic of disseminated intravascular coagulation (DIC), the sepsis-associated coagulopathy. Many of the pathogens, both bacterial and viral, that cause sepsis also directly activate platelets, which suggests that pathogen-induced platelet activation leads to systemic thrombosis and drives the multi-organ failure of DIC. In this paper we review the mechanisms of platelet activation by pathogens and the evidence for a role for anti-platelet agents in the management of sepsis.

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Section: Pathogen Interaction With Platelet Haemostasis Receptorsmentioning

confidence: 99%

Sepsis – it is all about the platelets

Cox

2023

Front. Immunol.

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Vascular tropism models of blood-borne microbial dissemination

Ebady

et al. 2021

Preprint

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SUMMARYSimilar to circulating tumour and immune cells, many blood-borne microbes preferentially “home” to specific vascular sites and tissues during hematogenous dissemination 1–5. For many pathogens, the “postal codes” and mechanisms responsible for tissue-specific vascular tropism are unknown and have been challenging to unravel. Members of the Lyme disease Borreliella burgdorferi species complex infect a broad range of mammalian tissues and exhibit complex strain-, species- and host-specific tissue tropism patterns. Intravenous perfusion experiments and intravital microscopy studies suggest that heterogeneous tissue tropism properties may depend on tissue-specific differences in host and microbial molecules supporting vascular interaction and extravasation. However, interpreting these studies can be complicated because of the immune-protective moonlighting (multitasking) properties of many B. burgdorferi adhesins. Here, we investigated whether B. burgdorferi vascular interaction properties measured by live cell imaging and particle tracking in aorta, bladder, brain, joint and skin microvascular flow chamber models predict strain- and tissue-specific dissemination patterns in vivo These studies identified strain- and endothelial cell type-specific interaction properties that accurately predicted in vivo dissemination of B. burgdorferi to bladder, brain, joint and skin but not aorta, and indicated that dissemination mechanisms in all of these tissues are distinct. Thus, the ability to interact with vascular surfaces under physiological shear stress is a key determinant of tissue-specific tropism for Lyme disease bacteria. The methods and model systems reported here will be invaluable for identifying and characterizing the diverse, largely undefined molecules and mechanisms supporting dissemination of Lyme disease bacteria. These methods and models may be useful for studying tissue tropism and vascular dissemination mechanisms of other blood-borne microbes.

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BBB07 contributes to, but is not essential for, Borrelia burgdorferi infection in mice

Cited by 2 publications

References 15 publications

Sepsis – it is all about the platelets

Sepsis – it is all about the platelets

Vascular tropism models of blood-borne microbial dissemination

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