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10.1186/s13075-018-1568-1 http://scihub22266oqcxt.onion/10.1186/s13075-018-1568-1 C5894134!5894134 !29636091     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29636091 &cmd=llinks): Failed to open stream: HTTP request failed! 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Dysregulated heme oxygenase-1(low) M2-like macrophages augment lupus nephritis via Bach1 induced by type I interferons |pdf=|usr=}}{{29636091 }} gab.com Text Dysregulated heme oxygenase-1(low) M2-like macrophages augment lupus nephritis via Bach1 induced by type I interferons JO: Arthritis Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=29636091 #FOAvip BACKGROUND: Innate immunity including macrophages (M?) in lupus nephritis (LN) has been gaining attention, but roles of M? 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 M? 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 M?, 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 M? correlated with the amounts of proteinuria in patients with LN. Unlike monocyte-derived M2-like M?, HO-1 expression was defective in the majority of glomerular M2-like M? of patients with LN. Stimulation of human M2-like M? 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 M? from Bach1-deficient MRL/lpr mice. CONCLUSIONS: Our data suggest that dysregulated M2-like M? play a proinflammatory role in LN. Bach1 is a potential therapeutic target that could restore the anti-inflammatory property of M2 M?. Twit Text FOAVip Dysregulated heme oxygenase-1(low) M2-like macrophages augment lupus nephritis via Bach1 induced by type I interferons ????Arthritis Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=29636091 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29636091 #FOAvip English Wikipedia <ref>{{Cite pmid|29636091 }}</ref> Dysregulated heme oxygenase-1(low) M2-like macrophages augment lupus nephritis via Bach1 induced by type I interferons #MMPMID29636091 Kishimoto D ; Kirino Y ; Tamura M ; Takeno M ; Kunishita Y ; Takase-Minegishi K ; Nakano H ; Kato I ; Nagahama K ; Yoshimi R ; Igarashi K ; Aoki I ; Nakajima H Arthritis Res Ther 2018[Apr]; 20 (1 ): 64 PMID29636091 show ga BACKGROUND: Innate immunity including macrophages (M?) in lupus nephritis (LN) has been gaining attention, but roles of M? 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 M? 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 M?, 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 M? correlated with the amounts of proteinuria in patients with LN. Unlike monocyte-derived M2-like M?, HO-1 expression was defective in the majority of glomerular M2-like M? of patients with LN. Stimulation of human M2-like M? 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 M? from Bach1-deficient MRL/lpr mice. CONCLUSIONS: Our data suggest that dysregulated M2-like M? play a proinflammatory role in LN. Bach1 is a potential therapeutic target that could restore the anti-inflammatory property of M2 M?. |Adult [MESH] |Animals [MESH] |Basic-Leucine Zipper Transcription Factors/*deficiency [MESH] |Cells, Cultured [MESH] |Female [MESH] |Heme Oxygenase-1/antagonists & inhibitors/*biosynthesis [MESH] |Humans [MESH] |Interferon Type I/*pharmacology [MESH] |Lupus Nephritis/*metabolism/pathology [MESH] |Macrophages/drug effects/*metabolism/pathology [MESH] |Male [MESH] |Membrane Proteins/antagonists & inhibitors/*biosynthesis [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH]Dysregulated heme oxygenase-1(low) M2-like macrophages augment lupus n(epmc).pdf DeepDyve Pubget Overpricing