B
Björn Petri
Researcher at University of Calgary
Publications - 46
Citations - 4196
Björn Petri is an academic researcher from University of Calgary. The author has contributed to research in topics: Vascular permeability & Leukocyte Rolling. The author has an hindex of 25, co-authored 46 publications receiving 3488 citations. Previous affiliations of Björn Petri include University of Münster & Max Planck Society.
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Journal ArticleDOI
Infection-induced NETosis is a dynamic process involving neutrophil multitasking in vivo
Bryan G. Yipp,Björn Petri,Davide Salina,Craig N. Jenne,Brittney N V Scott,Lori Zbytnuik,Keir Pittman,Muhammad Asaduzzaman,Kaiyu Wu,H. Christopher Meijndert,Stephen E. Malawista,Anne de Boisfleury Chevance,Kunyan Zhang,John Conly,Paul Kubes +14 more
TL;DR: Early in infection NETosis involves neutrophils that do not undergo lysis and retain the ability to multitask, and a requirement for both Toll-like receptor 2 and complement-mediated opsonization tightly regulated NET release.
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A dynamic spectrum of monocytes arising from the in situ reprogramming of CCR2+ monocytes at a site of sterile injury
Daniela Dal-Secco,Jing Wang,Zhutian Zeng,Elzbieta Kolaczkowska,Connie H.Y. Wong,Björn Petri,Richard M. Ransohoff,Israel F. Charo,Craig N. Jenne,Paul Kubes +9 more
TL;DR: In response to sterile liver injury, CCR2hiCX3CR1low inflammatory monocytes infiltrate the liver and form a ringlike structure around the injury site; this phenotypic transition was required for optimal repair.
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Nucleation of platelets with blood-borne pathogens on Kupffer cells precedes other innate immunity and contributes to bacterial clearance
TL;DR: This study identifies a previously unknown surveillance mechanism by which platelets survey macrophages that rapidly converts to a critical host response to blood-borne bacteria.
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The physiology of leukocyte recruitment: an in vivo perspective.
TL;DR: The mechanisms of leukocyte recruitment have been studied extensively in vitro and have shed light on the basic molecular structure-function relationship of adhesion and signaling molecules involved in this essential immune response, and physiological results that might not have been predicted from in vitro are highlighted.
Journal ArticleDOI
ESAM supports neutrophil extravasation, activation of Rho, and VEGF-induced vascular permeability
Frank Wegmann,Björn Petri,Alexander G. Khandoga,Christian Moser,Andrej Khandoga,Stefan Volkery,Hang Li,Ines Nasdala,Oliver Brandau,Reinhard Fässler,Stefan Butz,Fritz Krombach,Dietmar Vestweber +12 more
TL;DR: In this article, the authors showed that ESAM deficiency-related inhibitory effect on neutrophil extravasation was observed in mice carrying a disrupted ESAM gene and analyzed them in three different inflammation models, finding that recruitment of lymphocytes into inflamed skin was unaffected by the gene disruption.