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Colonization of dermal arterioles by Neisseria meningitidis provides a safe haven from neutrophils

Valeria Manriquez, Pierre Nivoit, Tomas Urbina, Hebert Echenique-Rivera, Keira Melican, Patricia Flamant, Taliah Schmitt, Patrick Bruneval, View ORCID ProfileDorian Obino, Guillaume Duménil
doi: https://doi.org/10.1101/2021.01.07.425689
Valeria Manriquez
1Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur, 75015 Paris, France
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Pierre Nivoit
1Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur, 75015 Paris, France
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Tomas Urbina
1Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur, 75015 Paris, France
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Hebert Echenique-Rivera
1Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur, 75015 Paris, France
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Keira Melican
1Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur, 75015 Paris, France
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Patricia Flamant
2Experimental Neuropathology Unit, Institut Pasteur, 75015 Paris, France
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Taliah Schmitt
3Paris Saint-Joseph Hospital, 75015 Paris, France
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Patrick Bruneval
4Service d’Anatomie Pathologie, Hôpital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France
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Dorian Obino
1Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur, 75015 Paris, France
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  • ORCID record for Dorian Obino
  • For correspondence: guillaume.dumenil@pasteur.fr dorian.obino@pasteur.fr
Guillaume Duménil
1Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur, 75015 Paris, France
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  • For correspondence: guillaume.dumenil@pasteur.fr dorian.obino@pasteur.fr
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Abstract

Neisseria meningitidis, a human-specific bacterium, is responsible for meningitis and fatal fulminant systemic disease. Bacteria colonize blood vessels, rapidly causing devastating vascular damage despite a neutrophil-rich inflammatory infiltrate. How this pathogen escapes the neutrophil response is unknown. Using a humanized mouse model, we show that vascular colonization leads to the recruitment of neutrophils, partially reducing bacterial burden and vascular damage. This partial effect is due to the ability of bacteria to indiscriminately colonize capillaries, venules and arterioles, as observed in human samples. In venules, potent neutrophil recruitment allows efficient bacterial phagocytosis. In contrast, in infected capillaries and arterioles adhesion molecules such as E-Selectin are not expressed on the endothelium and intravascular neutrophil recruitment is minimal. These results show that colonization of capillaries and arterioles by N. meningitidis create an intravascular niche that preclude the action of neutrophils, resulting in immune escape and subsequent fulminant progression of the infection.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted January 07, 2021.
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Colonization of dermal arterioles by Neisseria meningitidis provides a safe haven from neutrophils
Valeria Manriquez, Pierre Nivoit, Tomas Urbina, Hebert Echenique-Rivera, Keira Melican, Patricia Flamant, Taliah Schmitt, Patrick Bruneval, Dorian Obino, Guillaume Duménil
bioRxiv 2021.01.07.425689; doi: https://doi.org/10.1101/2021.01.07.425689
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Colonization of dermal arterioles by Neisseria meningitidis provides a safe haven from neutrophils
Valeria Manriquez, Pierre Nivoit, Tomas Urbina, Hebert Echenique-Rivera, Keira Melican, Patricia Flamant, Taliah Schmitt, Patrick Bruneval, Dorian Obino, Guillaume Duménil
bioRxiv 2021.01.07.425689; doi: https://doi.org/10.1101/2021.01.07.425689

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