NDLI: Dysregulated heme oxygenase-1low M2-like macrophages augment lupus nephritis via Bach1 induced by type I interferons

Content Provider	Springer Nature : BioMed Central
Author	Kishimoto, Daiga Kirino, Yohei Tamura, Maasa Takeno, Mitsuhiro Kunishita, Yosuke Takase-Minegishi, Kaoru Nakano, Hiroto Kato, Ikuma Nagahama, Kiyotaka Yoshimi, Ryusuke Igarashi, Kazuhiko Aoki, Ichiro Nakajima, Hideaki
Abstract	Background Innate immunity including macrophages (Mϕ) in lupus nephritis (LN) has been gaining attention, but roles of Mϕ in LN remain uncertain. Methods Immunohistochemical staining was performed to determine CD68, CD163, heme oxygenase (HO)-1 (a stress-inducible heme-degrading enzyme with anti-inflammatory property), pSTAT1, and CMAF-expressing Mϕ in the glomeruli of patients with LN. Effects of type I interferons on the expression levels of CD163, HO-1, BTB and CNC homology 1 (Bach1; a transcriptional HO-1 repressor), interleukin (IL)-6, and IL-10 by human M2-like Mϕ, which were differentiated in vitro from peripheral monocytes with macrophage colony-stimulating factor, were assessed by RT-PCR and immunocytostaining. Clinical manifestations, anti-double-stranded DNA (anti-dsDNA), and local HO-1 expression were compared in Bach1-deficient and wild-type MRL/lpr mice. Results The number of glomerular M2-like Mϕ correlated with the amounts of proteinuria in patients with LN. Unlike monocyte-derived M2-like Mϕ, HO-1 expression was defective in the majority of glomerular M2-like Mϕ of patients with LN. Stimulation of human M2-like Mϕ with type I interferons led to reduced HO-1 expression and increased Bach1 and IL-6 expression. Bach1-deficient MRL/lpr mice exhibited increased HO-1 expression in kidneys, prolonged survival, reduced urine proteins, and serum blood urea nitrogen levels, but serum anti-dsDNA antibody levels were comparable. Increased expression of CD163 and HO-1 was found in peritoneal Mϕ from Bach1-deficient MRL/lpr mice. Conclusions Our data suggest that dysregulated M2-like Mϕ play a proinflammatory role in LN. Bach1 is a potential therapeutic target that could restore the anti-inflammatory property of M2 Mϕ.
Related Links	https://arthritis-research.biomedcentral.com/counter/pdf/10.1186/s13075-018-1568-1.pdf
Ending Page	11
Page Count	11
Starting Page	1
File Format	HTM / HTML
ISSN	14786362
DOI	10.1186/s13075-018-1568-1
Journal	Arthritis Research & Therapy
Issue Number	1
Volume Number	20
Language	English
Publisher	BioMed Central
Publisher Date	2018-04-10
Access Restriction	Open
Subject Keyword	Rheumatology Orthopedics Lupus nephritis Heme oxygenase 1 Bach1 Type I interferons Macrophage polarization
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology Rheumatology
Journal Impact Factor	4.4/2023
5-Year Journal Impact Factor	4.9/2023

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