Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

The antibacterial defense against infections depends on the cooperation between distinct phagocytes of the innate immune system, namely macrophages and neutrophils. However, the mechanisms driving this cooperation are incompletely understood. In this study we describe the crosstalk between Ly6C⁺ and Ly6C(-) macrophage-subtypes and neutrophils in the context of urinary tract infection (UTI) with uropathogenic E. coli (UPEC). Ly6C(-) macrophages acted as tissue resident sentinels and attracted circulating phagocytes by chemokines. Ly6C⁺ macrophages produced tumor necrosis factor (TNF) that licensed Ly6C(-) macrophages to release preformed CXCL2, which in turn caused matrix metalloproteinases (MMP-9) secretion by neutrophils to enable transepithelial migration.

Original publication

DOI

10.3390/pathogens5010015

Type

Journal article

Journal

Pathogens (basel, switzerland)

Publication Date

02/2016

Volume

5

Addresses

Institute of Experimental Immunology and Imaging, Department Immunodynamics, University Hospital Essen, University Duisburg-Essen, Essen 45141, Germany. kristina.zec@uk-essen.de.