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

Valeria Manriquez, Pierre Nivoit, Tomas Urbina, Hebert Echenique-Rivera, Keira Melican, Marie-Paule Fernandez-Gerlinger, Patricia Flamant, Taliah Schmitt, Patrick Bruneval, Dorian Obino () and Guillaume Duménil ()
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Valeria Manriquez: Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur
Pierre Nivoit: Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur
Tomas Urbina: Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur
Hebert Echenique-Rivera: Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur
Keira Melican: Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur
Marie-Paule Fernandez-Gerlinger: Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur
Patricia Flamant: Experimental Neuropathology Unit, Institut Pasteur
Taliah Schmitt: Paris Saint-Joseph Hospital
Patrick Bruneval: Service d’Anatomie Pathologie, Hôpital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris (AP-HP)
Dorian Obino: Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur
Guillaume Duménil: Pathogenesis of Vascular Infections unit, INSERM, Institut Pasteur

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: Abstract The human pathogen Neisseria meningitidis can cause meningitis and fatal systemic disease. The bacteria colonize blood vessels and rapidly cause vascular damage, despite a neutrophil-rich inflammatory infiltrate. Here, we use a humanized mouse model to show that vascular colonization leads to the recruitment of neutrophils, which partially reduce bacterial burden and vascular damage. This partial effect is due to the ability of bacteria to 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. Our results indicate that the colonization of capillaries and arterioles by N. meningitidis creates an intravascular niche that precludes the action of neutrophils, resulting in immune escape and progression of the infection.

Date: 2021
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DOI: 10.1038/s41467-021-24797-z

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