Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2017 Nov 30;7:16628. doi: 10.1038/s41598-017-16778-4

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Working model of neutrophil-macrophage crosstalk via NET-bound HMGB1 during activation of neutrophils by mineralo-organic particles. When exposed to mineral particles, neutrophils interact with the particulate matters, which in turn lead to ROS production and NETosis. The released NETs deliver danger signals to bystander macrophages via NET-bound HMGB1. The NET-bound HMGB1 signals via a TLR2/TLR4-dependent pathway and initiates pro-inflammatory signaling cascades in the macrophages, resulting in inflammation via secretion of TNF-α.