Necrotic cell death increases the release of macrophage migration inhibitory factor by monocytes/macrophages

被引：17

作者：

Dankers, Wendy ^{[1
]}

Abul Hasnat, Md ^{[1
]}

Swann, Vanesa ^{[1
]}

Alharbi, Arwaf ^{[2
,3
]}

Lee, Jacinta P. W. ^{[1
,4
]}

Cristofaro, Megan A. ^{[1
]}

Gantier, Michael P. ^{[2
,3
]}

Jones, Sarah A. ^{[1
]}

Morand, Eric F. ^{[1
]}

Flynn, Jacqueline K. ^{[1
,5
]}

Harris, James ^{[1
]}

机构：

[1] Monash Univ, Fac Med Nursing & Hlth Sci, Ctr Inflammatory Dis, Sch Clin Sci,Monash Hlth,Rheumatol Res Grp, Clayton, Vic, Australia

[2] Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic, Australia

[3] Monash Univ, Dept Mol & Translat Sci, Clayton, Vic, Australia

[4] Univ Cambridge, Dept Med, Cambridge, England

[5] Univ Melbourne, Dept Microbiol & Immunol, Peter Doherty Inst Infect & Immun, Melbourne, Vic, Australia

来源：

IMMUNOLOGY AND CELL BIOLOGY | 2020年 / 98卷 / 09期

关键词：

cytokines; inflammasome; inflammation; necroptosis; necrosis; pyroptosis; MIF; RECEPTORS; CYTOKINE; VITRO;

D O I：

10.1111/imcb.12376

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Macrophage migration inhibitory factor (MIF) is a pleiotropic inflammatory molecule with both cytokine and noncytokine activity. MIF is constitutively released from multiple cell types via an unconventional secretory pathway that is not well defined. Here, we looked at MIF release from human and mouse monocytes/macrophages in response to different stimuli. While MIF release was not significantly altered in response to lipopolysaccharide or heat-killedEscherichia coli, cytotoxic stimuli strongly promoted release of MIF. MIF release was highly upregulated in cells undergoing necrosis, necroptosis and NLRP3 inflammasome-dependent pyroptosis. Our data suggest that cell death represents a major route for MIF release from myeloid cells. The functional significance of these findings and their potential importance in the context of autoimmune and inflammatory diseases warrant further investigation.

引用

页码：782 / 790

页数：9

共 30 条

[1] MIF interacts with CXCR7 to promote receptor internalization, ERK1/2 and ZAP-70 signaling, and lymphocyte chemotaxis [J].

Alampour-Rajabi, Setareh ;

El Bounkari, Omar ;

Rot, Antal ;

Mueller-Newen, Gerhard ;

Bachelerie, Francoise ;

Gawaz, Meinrad ;

Weber, Christian ;

Schober, Andreas ;

Bernhagen, Juergen .

FASEB JOURNAL, 2015, 29 (11) :4497-4511

[2] MIF and D-DT are potential disease severity modifiers in male MS subjects [J].

Benedek, Gil ;

Meza-Romero, Roberto ;

Jordan, Kelley ;

Zhang, Ying ;

Nguyen, Ha ;

Kent, Gail ;

Li, Jia ;

Siu, Edwin ;

Frazer, Jenny ;

Piecychna, Marta ;

Du, Xin ;

Sreih, Antoine ;

Leng, Lin ;

Wiedrick, Jack ;

Caillier, Stacy J. ;

Offner, Halina ;

Oksenberg, Jorge R. ;

Yadav, Vijayshree ;

Bourdette, Dennis ;

Bucala, Richard ;

Vandenbark, Arthur A. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2017, 114 (40) :E8421-E8429

[3] MIF IS A PITUITARY-DERIVED CYTOKINE THAT POTENTIATES LETHAL ENDOTOXEMIA [J].

BERNHAGEN, J ;

CALANDRA, T ;

MITCHELL, RA ;

MARTIN, SB ;

TRACEY, KJ ;

VOELTER, W ;

MANOGUE, KR ;

CERAMI, A ;

BUCALA, R .

NATURE, 1993, 365 (6448) :756-759

[4] PURIFICATION, BIOACTIVITY, AND SECONDARY STRUCTURE-ANALYSIS OF MOUSE AND HUMAN MACROPHAGE-MIGRATION INHIBITORY FACTOR (MIF) [J].

BERNHAGEN, J ;

MITCHELL, RA ;

CALANDRA, T ;

VOELTER, W ;

CERAMI, A ;

BUCALA, R .

BIOCHEMISTRY, 1994, 33 (47) :14144-14155

[5] MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment [J].

Bernhagen, Juergen ;

Krohn, Regina ;

Lue, Hongqi ;

Gregory, Julia L. ;

Zernecke, Alma ;

Koenen, Rory R. ;

Dewor, Manfred ;

Georgiev, Ivan ;

Schober, Andreas ;

Leng, Lin ;

Kooistra, Teake ;

Fingerle-Rowson, Guenter ;

Ghezzi, Pietro ;

Kleemann, Robert ;

McColl, Shaun R. ;

Bucala, Richard ;

Hickey, Michael J. ;

Weber, Christian .

NATURE MEDICINE, 2007, 13 (05) :587-596

[6] MECHANISM OF A REACTION IN VITRO ASSOCIATED WITH DELAYED-TYPE HYPERSENSITIVITY [J].

BLOOM, BR ;

BENNETT, B .

SCIENCE, 1966, 153 (3731) :80-&

[7] MACROPHAGE IS AN IMPORTANT AND PREVIOUSLY UNRECOGNIZED SOURCE OF MACROPHAGE-MIGRATION INHIBITORY FACTOR [J].

CALANDRA, T ;

BERNHAGEN, J ;

MITCHELL, RA ;

BUCALA, R .

JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 179 (06) :1895-1902

[8] Macrophage migration inhibitory factor is a critical mediator of the activation of immune cells by exotoxins of gram-positive bacteria [J].

Calandra, T ;

Spiegel, LA ;

Metz, CN ;

Bucala, R .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (19) :11383-11388

[9] Protection from septic shock by neutralization of macrophage migration inhibitory factor [J].

Calandra, T ;

Echtenacher, B ;

Le Roy, D ;

Pugin, J ;

Metz, CN ;

Hültner, L ;

Heumann, D ;

Männel, D ;

Bucala, R ;

Glauser, MP .

NATURE MEDICINE, 2000, 6 (02) :164-170

[10] MIF AS A GLUCOCORTICOID-INDUCED MODULATOR OF CYTOKINE PRODUCTION [J].

CALANDRA, T ;

BERNHAGEN, J ;

METZ, CN ;

SPIEGEL, LA ;

BACHER, M ;

DONNELLY, T ;

CERAMI, A ;

BUCALA, R .

NATURE, 1995, 377 (6544) :68-71

← 1 2 3 →