EGCG induces G-CSF expression and neutrophilia in experimental sepsis

Publication Date

2015

Journal Title

Immunol Res

Abstract

A major green tea component, epigallocatechin-3-gallate (EGCG), has been proven protective against lethal sepsis in experimental setting, but its protective mechanisms remain incompletely understood. Here, we provide evidence to support EGCG's capacities in stimulating G-CSF production and neutrophilia in vivo. In an animal model of sepsis, EGCG significantly elevated peritoneal levels of G-CSF and several chemokines (e.g., MCP-1/CCL2 and MIP-1gamma/CCL9), and consequently increased peritoneal neutrophil numbers (neutrophilia) at a late stage. In vitro, EGCG divergently affected HMGB1-mediated production of several chemokines: reducing CXCL15 and RANTES/CCL5, but elevating G-CSF and MIP-1alpha/CCL3 production by peritoneal macrophages. Similarly, it significantly induced the expression and secretion of G-CSF and MIP-1alpha/CCL3 in human peripheral blood mononuclear cells. Based on our preliminary data, it may be important to search for anti-inflammatory and G-CSF-stimulating agents for the clinical management of inflammatory diseases.

Volume Number

63

Issue Number

1-3

Pages

144-52

Document Type

Article

EPub Date

2015/08/22

Status

Faculty, Northwell Researcher

Facility

School of Medicine; Northwell Health

Primary Department

Emergency Medicine

Additional Departments

Otolaryngology

PMID

26293782

DOI

10.1007/s12026-015-8681-x

For the public and Northwell Health campuses

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