Eosinophils Oxidize Damage-Associated Molecular Pattern Molecules Derived from Stressed Cells

被引:83
|
作者
Lotfi, Ramin [1 ]
Herzog, Gloria Isabelle [1 ]
DeMarco, Richard Anthony [5 ]
Beer-Stolz, Donna [3 ]
Lee, James Joseph [4 ]
Rubartelli, Anna [2 ]
Schrezenmeier, Hubert [1 ]
Lotze, Michael Thomas [3 ]
机构
[1] Univ Ulm, Inst Transfus Med, Inst Klin Transfus Med & Immungenet Ulm, Ulm, Germany
[2] Inst Natl Ric Cancro, Cell Biol Lab, Genoa, Italy
[3] Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15213 USA
[4] Mayo Clin Scottsdale, Dept Biochem & Mol Biol, Scottsdale, AZ 85259 USA
[5] Amnis Corp, Seattle, WA 98121 USA
来源
JOURNAL OF IMMUNOLOGY | 2009年 / 183卷 / 08期
关键词
GROUP BOX-1 PROTEIN; ALLERGIC PULMONARY INFLAMMATION; NADPH OXIDASE COMPONENTS; MAJOR BASIC-PROTEIN; IMMUNE-RESPONSE; CANCER-PATIENTS; ACTIVATION; RELEASE; HMGB1; DEGRANULATION;
D O I
10.4049/jimmunol.0900504
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Eosinophils (Eos) are found at increased numbers within necrotic areas of tumors. We show that necrotic material from cell lysates containing damage-associated molecular pattern molecules induce eosinophil degranulation (release of major basic protein and eosinophil peroxidase) and enhance their oxidative burst while the stimulatory capacity of cell lysates is significantly diminished following oxidation. High mobility group box 1 (HMGB1), a prototypic damage-associated molecular pattern molecule, released following necrosis but not apoptosis, induced a similar effect on Eos. Additionally, we demonstrate that HMGB1 enhances eosinophil survival and acts as a chemoattractant. Consistently, we show that Eos express an HMGB1 receptor, the receptor for advanced glycation end product, and that anti-receptor for advanced glycation end product could diminish the HMGB1-mediated effects. Of all tested biologic activities, Eos respond most sensitively to the presence of necrotic material including HMGB1 with generation of peroxide. We postulate that Eos "sense" necrotic cell death, migrating to and responding to areas of tissue injury/necrosis. Oxidation of cell lysates reduces their biologic activity when compared with native lysates. We postulate that eosinophil-associated modulation of immunity within tumor and other damaged tissues may be primarily by promoting oxidative degradation of necrotic material. Novel therapeutic strategies may be considered by advancing oxidative denaturation of released necrotic material using Eos or other aerobic strategies. The Journal of Immunology, 2009, 183: 5023-5031.
引用
收藏
页码:5023 / 5031
页数:9
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