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Article ; Online: Interplay of Heme with Macrophages in Homeostasis and Inflammation

Pooja Pradhan / Vijith Vijayan / Faikah Gueler / Stephan Immenschuh

International Journal of Molecular Sciences, Vol 21, Iss 3, p

2020 Volume 740

Abstract: Macrophages are an integral part of the mononuclear phagocyte system that is critical for maintaining immune homeostasis. They play a key role for initiation and modulation of immunological responses in inflammation and infection. Moreover, macrophages ... ...

Abstract	Macrophages are an integral part of the mononuclear phagocyte system that is critical for maintaining immune homeostasis. They play a key role for initiation and modulation of immunological responses in inflammation and infection. Moreover, macrophages exhibit a wide spectrum of tissue-specific phenotypes in steady-state and pathophysiological conditions. Recent clinical and experimental evidence indicates that the ubiquitous compound heme is a crucial regulator of these cells, e.g., in the differentiation of monocytes to tissue-resident macrophages and/ or in activation by inflammatory stimuli. Notably, heme, an iron containing tetrapyrrole, is essential as a prosthetic group of hemoproteins (e.g., hemoglobin and cytochromes), whereas non-protein bound free or labile heme can be harmful via pro-oxidant, pro-inflammatory, and cytotoxic effects. In this review, it will be discussed how the complex interplay of heme with macrophages regulates homeostasis and inflammation via modulating macrophage inflammatory characteristics and/ or hematopoiesis. A particular focus will be the distinct roles of intra- and extracellular labile heme and the regulation of its availability by heme-binding proteins. Finally, it will be addressed how heme modulates macrophage functions via specific transcriptional factors, in particular the nuclear repressor BTB and CNC homologue (BACH)1 and Spi-C.
Keywords	bach1 ; heme ; heme-binding proteins ; inflammation ; macrophages ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	612
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Genetic BACH1 deficiency alters mitochondrial function and increases NLRP3 inflammasome activation in mouse macrophages

Pooja Pradhan / Vijith Vijayan / Karsten Cirksena / Falk F.R. Buettner / Kazuhiko Igarashi / Roberto Motterlini / Roberta Foresti / Stephan Immenschuh

Redox Biology, Vol 51, Iss , Pp 102265- (2022)

2022

Abstract: BTB-and-CNC homologue 1 (BACH1), a heme-regulated transcription factor, mediates innate immune responses via its functional role in macrophages. BACH1 has recently been shown to modulate mitochondrial metabolism in cancer cells. In the current study, we ... ...

Abstract	BTB-and-CNC homologue 1 (BACH1), a heme-regulated transcription factor, mediates innate immune responses via its functional role in macrophages. BACH1 has recently been shown to modulate mitochondrial metabolism in cancer cells. In the current study, we utilized a proteomics approach and demonstrate that genetic deletion of BACH1 in mouse macrophages is associated with decreased levels of various mitochondrial proteins, particularly mitochondrial complex I. Bioenergetic studies revealed alterations of mitochondrial energy metabolism in BACH1−/− macrophages with a shift towards increased glycolysis and decreased oxidative phosphorylation. Moreover, these cells exhibited enhanced mitochondrial membrane potential and generation of mitochondrial reactive oxygen species (mtROS) along with lower levels of mitophagy. Notably, a higher inducibility of NLRP3 inflammasome activation in response to ATP and nigericin following challenge with lipopolysaccharide (LPS) was observed in BACH1-deficient macrophages compared to wild-type cells. Mechanistically, pharmacological inhibition of mtROS markedly attenuated inflammasome activation. In addition, it is shown that inducible nitric oxide synthase and cyclooxygenase-2, both of which are markedly induced by LPS in macrophages, are directly implicated in BACH1-dependent regulation of NLRP3 inflammasome activation. Taken together, the current findings indicate that BACH1 is critical for immunomodulation of macrophages and may serve as a target for therapeutic approaches in inflammatory disorders.
Keywords	BACH1 ; Mitochondrial metabolism ; Inflammation ; Macrophages ; Mitochondrial complex 1 ; NLRP3 inflammasome ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A Single Oral Dose of Diclofenac Causes Transition of Experimental Subclinical Acute Kidney Injury to Chronic Kidney Disease

Johanna Störmer / Wilfried Gwinner / Katja Derlin / Stephan Immenschuh / Song Rong / Mi-Sun Jang / Nelli Shushakova / Hermann Haller / Faikah Gueler / Robert Greite

Biomedicines, Vol 10, Iss 1198, p

2022 Volume 1198

Abstract: Nephrotoxic drugs can cause acute kidney injury (AKI) and analgesic nephropathy. Diclofenac is potentially nephrotoxic and frequently prescribed for pain control. In this study, we investigated the effects of single and repetitive oral doses of ... ...

Abstract	Nephrotoxic drugs can cause acute kidney injury (AKI) and analgesic nephropathy. Diclofenac is potentially nephrotoxic and frequently prescribed for pain control. In this study, we investigated the effects of single and repetitive oral doses of diclofenac in the setting of pre-existing subclinical AKI on the further course of AKI and on long-term renal consequences. Unilateral renal ischemia–reperfusion injury (IRI) for 15 min was performed in male CD1 mice to induce subclinical AKI. Immediately after surgery, single oral doses (100 mg or 200 mg) of diclofenac were administered. In a separate experimental series, repetitive treatment with 100 mg diclofenac over three days was performed after IRI and sham surgery. Renal morphology and pro-fibrotic markers were investigated 24 h and two weeks after the single dose and three days after the repetitive dose of diclofenac treatment using histology, immunofluorescence, and qPCR. Renal function was studied in a bilateral renal IRI model. A single oral dose of 200 mg, but not 100 mg, of diclofenac after IRI aggravated acute tubular injury after 24 h and caused interstitial fibrosis and tubular atrophy two weeks later. Repetitive treatment with 100 mg diclofenac over three days aggravated renal injury and caused upregulation of the pro-fibrotic marker fibronectin in the setting of subclinical AKI, but not in sham control kidneys. In conclusion, diclofenac aggravated renal injury in pre-existing subclinical AKI in a dose and time-dependent manner and already a single dose can cause progression to chronic kidney disease (CKD) in this model.
Keywords	acute kidney injury ; chronic kidney disease ; ischemia–reperfusion injury ; diclofenac nephrotoxicity ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Kidney injury after lung transplantation

Julian Doricic / Robert Greite / Vijith Vijayan / Stephan Immenschuh / Andreas Leffler / Fabio Ius / Axel Haverich / Jens Gottlieb / Hermann Haller / Irina Scheffner / Wilfried Gwinner

PLoS ONE, Vol 17, Iss 3, p e

Long-term mortality predicted by post-operative day-7 serum creatinine and few clinical factors.

2022 Volume 0265002

Abstract: Background Acute kidney injury (AKI) after lung transplantation (LuTx) is associated with increased long-term mortality. In this prospective observational study, commonly used AKI-definitions were examined regarding prediction of long-term mortality and ... ...

Abstract	Background Acute kidney injury (AKI) after lung transplantation (LuTx) is associated with increased long-term mortality. In this prospective observational study, commonly used AKI-definitions were examined regarding prediction of long-term mortality and compared to simple use of the serum creatinine value at day 7 for patients who did not receive hemodialysis, and serum creatinine value immediately before initiation of hemodialysis (d7/preHD-sCr). Methods 185 patients with LuTx were prospectively enrolled from 2013-2014 at our center. Kidney injury was assessed within 7 days by: (1) the Kidney Disease Improving Global Outcomes criteria (KDIGO-AKI), (2) the Acute Disease Quality Initiative 16 Workgroup classification (ADQI-AKI) and (3) d7/preHD-sCr. Prediction of all-cause mortality was examined by Cox regression analysis, and clinical as well as laboratory factors for impaired kidney function post-LuTx were analyzed. Results AKI according to KDIGO and ADQI-AKI occurred in 115 patients (62.2%) within 7 days after LuTx. Persistent ADQI-AKI, KDIGO-AKI stage 3 and higher d7/preHD-sCr were associated with higher mortality in the univariable analysis. In the multivariable analysis, d7/preHD-sCr in combination with body weight and intra- and postoperative platelet transfusions predicted mortality after LuTx with similar performance as models using KDIGO-AKI and ADQI-AKI (concordance index of 0.75 for d7/preHD-sCr vs., 0.74 and 0.73, respectively). Pre-transplant reduced renal function, diabetes, higher BMI, and intraoperative ECMO predicted higher d7/preHD-sCr (r2 = 0.354, p < 0.001). Conclusion Our results confirm the importance of AKI in lung transplant patients; however, a simple and pragmatic indicator of renal function, d7/preHD-sCr, predicts long-term mortality equally reliable as more complex AKI-definitions like KDIGO and ADQI.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Targeting the Heme-Heme Oxygenase System to Prevent Severe Complications Following COVID-19 Infections

Frank A.D.T.G. Wagener / Peter Pickkers / Stephen J. Peterson / Stephan Immenschuh / Nader G. Abraham

Antioxidants, Vol 9, Iss 540, p

2020 Volume 540

Abstract: SARS-CoV-2 is causing a pandemic resulting in high morbidity and mortality. COVID-19 patients suffering from acute respiratory distress syndrome (ARDS) are often critically ill and show lung injury and hemolysis. Heme is a prosthetic moiety crucial for ... ...

Abstract	SARS-CoV-2 is causing a pandemic resulting in high morbidity and mortality. COVID-19 patients suffering from acute respiratory distress syndrome (ARDS) are often critically ill and show lung injury and hemolysis. Heme is a prosthetic moiety crucial for the function of a wide variety of heme-proteins, including hemoglobin and cytochromes. However, injury-derived free heme promotes adhesion molecule expression, leukocyte recruitment, vascular permeabilization, platelet activation, complement activation, thrombosis, and fibrosis. Heme can be degraded by the anti-inflammatory enzyme heme oxygenase (HO) generating biliverdin/bilirubin, iron/ferritin, and carbon monoxide. We therefore postulate that free heme contributes to many of the inflammatory phenomena witnessed in critically ill COVID-19 patients, whilst induction of HO-1 or harnessing heme may provide protection. HO-activity not only degrades injurious heme, but its effector molecules possess also potent salutary anti-oxidative and anti-inflammatory properties. Until a vaccine against SARS-CoV-2 becomes available, we need to explore novel strategies to attenuate the pro-inflammatory, pro-thrombotic, and pro-fibrotic consequences of SARS-CoV-2 leading to morbidity and mortality. The heme-HO system represents an interesting target for novel “proof of concept” studies in the context of COVID-19.
Keywords	heme ; heme oxygenase ; SARS-CoV-2 ; inflammation ; COVID-19 ; Therapeutics. Pharmacology ; RM1-950 ; covid19
Subject code	612
Language	English
Publishing date	2020-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Human and murine macrophages exhibit differential metabolic responses to lipopolysaccharide - A divergent role for glycolysis

Vijith Vijayan / Pooja Pradhan / Laura Braud / Heiko R. Fuchs / Faikah Gueler / Roberto Motterlini / Roberta Foresti / Stephan Immenschuh

Redox Biology, Vol 22, Iss , Pp - (2019)

2019

Abstract: Macrophages adopt different phenotypes in response to microenvironmental changes, which can be principally classified into inflammatory and anti-inflammatory states. Inflammatory activation of macrophages has been linked with metabolic reprogramming from ...

Abstract	Macrophages adopt different phenotypes in response to microenvironmental changes, which can be principally classified into inflammatory and anti-inflammatory states. Inflammatory activation of macrophages has been linked with metabolic reprogramming from oxidative phosphorylation to aerobic glycolysis. In contrast to mouse macrophages, little information is available on the link between metabolism and inflammation in human macrophages. In the current report it is demonstrated that lipopolysaccharide (LPS)-activated human peripheral blood monocyte-derived macrophages (hMDMs) fail to undergo metabolic reprogramming towards glycolysis, but rely on oxidative phosphorylation for the generation of ATP. By contrast, activation by LPS led to an increased extracellular acidification rate (glycolysis) and decreased oxygen consumption rate (oxidative phosphorylation) in mouse bone marrow-derived macrophages (mBMDMs). Mitochondrial bioenergetics after LPS stimulation in human macrophages was unchanged, but was markedly impaired in mouse macrophages. Furthermore, treatment with 2-deoxyglucose, an inhibitor of glycolysis, led to cell death in mouse, but not in human macrophages. Finally, glycolysis appeared to be critical for LPS-mediated induction of the anti-inflammatory cytokine interleukin-10 in both human and mouse macrophages. In summary, these findings indicate that LPS-induced immunometabolism in human macrophages is different to that observed in mouse macrophages. Keywords: Bioenergetics, Inflammation, Macrophage, Metabolic reprogramming, Mitochondrial function
Keywords	Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2019-04-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Alpha1-antitrypsin counteracts heme-induced endothelial cell inflammatory activation, autophagy dysfunction and death

Kukuh Madyaningrana / Vijith Vijayan / Christoph Nikolin / Abid Aljabri / Srinu Tumpara / Elena Korenbaum / Harshit Shah / Metodi Stankov / Heiko Fuchs / Sabina Janciauskiene / Stephan Immenschuh

Redox Biology, Vol 46, Iss , Pp 102060- (2021)

2021

Abstract: Free heme toxicity in the vascular endothelium is critical for the pathogenesis of hemolytic disorders including sickle cell disease. In the current study, it is demonstrated that human alpha1-antitrypsin (A1AT), a serine protease inhibitor with high ... ...

Abstract	Free heme toxicity in the vascular endothelium is critical for the pathogenesis of hemolytic disorders including sickle cell disease. In the current study, it is demonstrated that human alpha1-antitrypsin (A1AT), a serine protease inhibitor with high binding-affinity for heme, rescues endothelial cell (EC) injury caused by free heme. A1AT provided endothelial protection against free heme toxicity via a pathway that differs from human serum albumin and hemopexin, two prototypical heme-binding proteins. A1AT inhibited heme-mediated pro-inflammatory activation and death of ECs, but did not affect the increase in intracellular heme levels and up-regulation of the heme-inducible enzyme heme oxygenase-1. Moreover, A1AT reduced heme-mediated generation of mitochondrial reactive oxygen species. Extracellular free heme led to an increased up-take of A1AT by ECs, which was detected in lysosomes and was found to reduce heme-dependent alkalization of these organelles. Finally, A1AT was able to restore heme-dependent dysfunctional autophagy in ECs. Taken together, our findings show that A1AT rescues ECs from free heme-mediated pro-inflammatory activation, cell death and dysfunctional autophagy. Hence, A1AT therapy may be useful in the treatment of hemolytic disorders such as sickle cell disease.
Keywords	alpha1-antitrypsin ; Endothelial cell ; Cell death ; Heme ; Heme-binding proteins ; Inflammation ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: An Antibody-Aptamer-Hybrid Lateral Flow Assay for Detection of CXCL9 in Antibody-Mediated Rejection after Kidney Transplantation

Lisa K. Seiler / Ngoc Linh Phung / Christoph Nikolin / Stephan Immenschuh / Christian Erck / Jessica Kaufeld / Hermann Haller / Christine S. Falk / Rebecca Jonczyk / Patrick Lindner / Stefanie Thoms / Julia Siegl / Günter Mayer / Regina Feederle / Cornelia A. Blume

Diagnostics, Vol 12, Iss 308, p

2022 Volume 308

Abstract: Chronic antibody-mediated rejection (AMR) is a key limiting factor for the clinical outcome of a kidney transplantation (Ktx), where early diagnosis and therapeutic intervention is needed. This study describes the identification of the biomarker CXC- ... ...

Abstract	Chronic antibody-mediated rejection (AMR) is a key limiting factor for the clinical outcome of a kidney transplantation (Ktx), where early diagnosis and therapeutic intervention is needed. This study describes the identification of the biomarker CXC-motif chemokine ligand (CXCL) 9 as an indicator for AMR and presents a new aptamer-antibody-hybrid lateral flow assay (hybrid-LFA) for detection in urine. Biomarker evaluation included two independent cohorts of kidney transplant recipients (KTRs) from a protocol biopsy program and used subgroup comparisons according to BANFF-classifications. Plasma, urine and biopsy lysate samples were analyzed with a Luminex-based multiplex assay. The CXCL9-specific hybrid-LFA was developed based upon a specific rat antibody immobilized on a nitrocellulose-membrane and the coupling of a CXCL9-binding aptamer to gold nanoparticles. LFA performance was assessed according to receiver operating characteristic (ROC) analysis. Among 15 high-scored biomarkers according to a neural network analysis, significantly higher levels of CXCL9 were found in plasma and urine and biopsy lysates of KTRs with biopsy-proven AMR. The newly developed hybrid-LFA reached a sensitivity and specificity of 71% and an AUC of 0.79 for CXCL9. This point-of-care-test (POCT) improves early diagnosis-making in AMR after Ktx, especially in KTRs with undetermined status of donor-specific HLA-antibodies.
Keywords	biomarkers ; antibody-mediated rejection (AMR) ; neural net analysis ; CXCL9 (MIG) ; aptamer ; antibody ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Heme oxygenase, inflammation, and fibrosis

StephanImmenschuh / DitteM. S.Lundvig

Frontiers in Pharmacology, Vol

the good, the bad, and the ugly?

2012 Volume 3

Abstract: Upon injury, prolonged inflammation and oxidative stress may cause pathological wound healing and fibrosis, leading to formation of excessive scar tissue. Fibrogenesis can occur in most organs and tissues and may ultimately lead to organ dysfunction and ... ...

Abstract	Upon injury, prolonged inflammation and oxidative stress may cause pathological wound healing and fibrosis, leading to formation of excessive scar tissue. Fibrogenesis can occur in most organs and tissues and may ultimately lead to organ dysfunction and failure. The underlying mechanisms of pathological wound healing still remains unclear, but are considered to have a multifactoral pathogenesis, and so far, no efficient anti-fibrotic therapies exists. Extra- and intracellular levels of free heme may be increased in a variety of pathological conditions due to heme-release from hemoproteins. Free heme possesses pro-inflammatory and oxidative effects, and may act as a danger signal, which counteracted by protein scavenging via various heme-binding proteins and by heme degradation. Heme is degraded by heme oxygenase (HO) that exists as two isoforms: inducible HO-1 and constitutively expressed HO-2. This generates the effector molecules biliverdin, carbon monoxide, and free iron. HO deficiency in mouse and man leads to exaggerated inflammation upon insults, and still accumulating epidemiological and preclinical studies support the widely recognized notion of the cytoprotective, anti-oxidative, and anti-inflammatory effects of the activity of the HO system and the generated effector molecules. In this review, we address the potential applications of targeted HO-1 induction or administration of its effector molecules as therapeutic targets in fibrotic and inflammatory conditions to counteract inflammatory and oxidative insults. This is shown in various clinically relevant conditions, such as hypertrophic scarring, chronic inflammatory liver disease, chronic pancreatitis, and chronic graft rejection in transplantation.
Keywords	Bilirubin ; Carbon Monoxide ; Fibrosis ; Heme ; heme oxygenase ; therapy ; Therapeutics. Pharmacology ; RM1-950 ; Medicine ; R
Subject code	610
Language	English
Publishing date	2012-05-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cell-Free Hemoglobin in Acute Kidney Injury after Lung Transplantation and Experimental Renal Ischemia/Reperfusion

International Journal of Molecular Sciences, Vol 23, Iss 13272, p

2022 Volume 13272

Abstract: Cell-free hemoglobin (CFH), a pro-oxidant and cytotoxic compound that is released in hemolysis, has been associated with nephrotoxicity. Lung transplantation (LuTx) is a clinical condition with a high incidence of acute kidney injury (AKI). In this study, ...

Abstract	Cell-free hemoglobin (CFH), a pro-oxidant and cytotoxic compound that is released in hemolysis, has been associated with nephrotoxicity. Lung transplantation (LuTx) is a clinical condition with a high incidence of acute kidney injury (AKI). In this study, we investigated the plasma levels of CFH and haptoglobin, a CFH-binding serum protein, in prospectively enrolled LuTx patients ( n = 20) with and without AKI. LuTx patients with postoperative AKI had higher CFH plasma levels at the end of surgery compared with no-AKI patients, and CFH correlated with serum creatinine at 48 h. Moreover, CFH levels inversely correlated with haptoglobin levels, which were significantly reduced at the end of surgery in LuTx patients with AKI. Because multiple other factors can contribute to AKI development in the complex clinical setting of LuTx, we next investigated the role of exogenous CFH administration in a mouse model of mild bilateral renal ischemia reperfusion injury (IRI). Exogenous administration of CFH after reperfusion caused overt AKI with creatinine increase, tubular injury, and enhanced markers of renal inflammation compared with vehicle-treated animals. In conclusion, CFH is a possible factor contributing to postoperative AKI after LuTx and promotes AKI in an experimental model of mild transient renal ischemia. Targeting CFH might be a therapeutic option to prevent AKI after LuTx.
Keywords	acute kidney injury ; free hemoglobin ; hemolysis ; lung transplantation ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610 ; 616
Language	English
Publishing date	2022-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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