Differential regulation of macrophage activation by the MIF cytokine superfamily members MIF and MIF-2 in adipose tissue during endotoxemia.
3T3 Cells
Adipocytes
/ metabolism
Adipose Tissue
/ cytology
Adipose Tissue, White
/ cytology
Animals
Cells, Cultured
Endotoxemia
/ immunology
Enzyme-Linked Immunosorbent Assay
Flow Cytometry
Intramolecular Oxidoreductases
/ genetics
Macrophage Activation
/ genetics
Macrophage Migration-Inhibitory Factors
/ genetics
Macrophages, Peritoneal
/ metabolism
Male
Mice
Mice, Inbred C57BL
D-DT
MIF
MIF-2
adipose tissue
inflammation
macrophage
macrophage polarization
sepsis
wound healing
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
18
06
2019
revised:
27
12
2019
accepted:
07
01
2020
pubmed:
22
1
2020
medline:
22
1
2021
entrez:
22
1
2020
Statut:
ppublish
Résumé
Sepsis is a leading cause of death worldwide and recent studies have shown white adipose tissue (WAT) to be an important regulator in septic conditions. In the present study, the role of the inflammatory cytokine macrophage migration inhibitory factor (MIF) and its structural homolog D-dopachrome tautomerase (D-DT/MIF-2) were investigated in WAT in a murine endotoxemia model. Both MIF and MIF-2 levels were increased in the peritoneal fluid of LPS-challenged wild-type mice, yet, in visceral WAT, the proteins were differentially regulated, with elevated MIF but downregulated MIF-2 expression in adipocytes. Mif gene deletion polarized adipose tissue macrophages (ATM) toward an anti-inflammatory phenotype while Mif-2 gene knockout drove ATMs toward a pro-inflammatory phenotype and Mif-deficiency was found to increase fibroblast viability. Additionally, we observed the same differential regulation of these two MIF family proteins in human adipose tissue in septic vs healthy patients. Taken together, these data suggest an inverse relationship between adipocyte MIF and MIF-2 expression during systemic inflammation, with the downregulation of MIF-2 in fat tissue potentially increasing pro-inflammatory macrophage polarization to further drive adipose inflammation.
Identifiants
pubmed: 31961019
doi: 10.1096/fj.201901511R
pmc: PMC7060131
mid: NIHMS1067841
doi:
Substances chimiques
Macrophage Migration-Inhibitory Factors
0
Intramolecular Oxidoreductases
EC 5.3.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
4219-4233Subventions
Organisme : NHLBI NIH HHS
ID : K08 HL135402
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR049610
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL130669
Pays : United States
Informations de copyright
© 2020 Federation of American Societies for Experimental Biology.
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