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Broadley, S.P.* ; Plaumann, A.* ; Coletti, R.* ; Lehmann, C.* ; Wanisch, A.* ; Seidlmeier, A.* ; Esser, K. ; Luo, S. ; Rämer, P.C.* ; Massberg, S.* ; Busch, D.H.* ; van Lookeren Campagne, M.* ; Verschoor, A.*

Dual-track clearance of circulating bacteria balances rapid restoration of blood sterility with induction of adaptive immunity.

Cell Host Microbe 20, 36-48 (2016)
Verlagsversion DOI PMC
Free by publisher
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Efficient clearance of bacteremia prevents life-threatening disease. Platelet binding to intravascular bacteria, a process involving platelet glycoprotein GPIb and bacterial opsonization with activated complement C3, influences blood clearance and anti-infective immunity. Using intravital microscopy of the bloodstream of mice infected with Listeria monocytogenes, we show that bacterial clearance is not a uniform process but a "dual-track" mechanism consisting of parallel "fast" and "slow" pathways. "Slow clearance" is regulated by time-dependent bacterial opsonization, stochastic platelet binding, and capture of bacteria-platelet-complexes via the complement receptor of the immunoglobulin superfamily, CRIg. The mechanism spares some bacteria from "fast clearance" and rapid destruction in the liver via Kupffer cell scavenger receptors, keeping them available for adaptive immunity induction by splenic CD8α(+) dendritic cells. We consistently find "fast" and "slow" clearance patterns for a broad panel of other Gram+ and Gram- bacteria. Thus, dual-track clearance balances rapid restoration of blood sterility with induction of specific antibacterial immunity.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Listeria-monocytogenes Infection; In-vivo Depletion; Dendritic Cells; Scavenger Receptors; Kupffer Cells; Complement; Liver; Mice; Macrophages; Responses
ISSN (print) / ISBN 1931-3128
e-ISSN 1934-6069
Zeitschrift Cell Host & Microbe
Quellenangaben Band: 20, Heft: 1, Seiten: 36-48 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort Cambridge
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Virology (VIRO)