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Article ; Online: Immunomodulatory roles of red blood cells.

Dobkin, Jane / Mangalmurti, Nilam S

2022 Volume 29, Issue 6, Page(s) 306–309

Abstract: Purpose of the review: To discuss recent advances supporting the role of red blood cells (RBCs) in the host immune response.: Recent findings: Over the last century, research has demonstrated that red blood cells exhibit functions beyond oxygen ... ...

Abstract	Purpose of the review: To discuss recent advances supporting the role of red blood cells (RBCs) in the host immune response. Recent findings: Over the last century, research has demonstrated that red blood cells exhibit functions beyond oxygen transport, including immune function. Recent work indicates that the nucleic acid sensing receptor, toll-like receptor 9 (TLR9), is expressed on the RBC surface and implicated in innate immune activation and red cell clearance during inflammatory states. In addition to this DNA-sensing role of RBCs, there is growing evidence that RBCs may influence immune function by inducing vascular dysfunction. RBC proteomics and metabolomics have provided additional insight into RBC immune function, with several studies indicating changes to RBC membrane structure and metabolism in response to severe acute respiratory syndrome coronavirus 2 infection. These structural RBC changes may even provide insight into the pathophysiology of the 'long-coronavirus disease 2019' phenomenon. Finally, evidence suggests that RBCs may influence host immune responses via complement regulation. Taken together, these recent findings indicate RBCs possess immune function. Further studies will be required to elucidate better how RBC immune function contributes to the heterogeneous host response during inflammatory states. Summary: The appreciation for nongas exchanging, red blood cell immune functions is rapidly growing. A better understanding of these RBC functions may provide insight into the heterogeneity observed in the host immune response to infection and inflammation.
MeSH term(s)	COVID-19 ; Erythrocytes/metabolism ; Humans ; Immunity ; Nucleic Acids/metabolism ; Oxygen/metabolism ; Toll-Like Receptor 9/metabolism
Chemical Substances	Nucleic Acids ; Toll-Like Receptor 9 ; Oxygen (S88TT14065)
Language	English
Publishing date	2022-07-18
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000734
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Article ; Online: The ultimate tradeoff: how red cell adaptations to malaria alter the host response during critical illness.

Dobkin, Jane / Wu, Ling / Mangalmurti, Nilam S

American journal of physiology. Lung cellular and molecular physiology

2023 Volume 324, Issue 2, Page(s) L169–L178

Abstract: The human immune system evolved in response to pathogens. Among these pathogens, malaria has proven to be one of the deadliest and has exerted the most potent selective pressures on its target cell, the red blood cell. Red blood cells have recently ... ...

Abstract	The human immune system evolved in response to pathogens. Among these pathogens, malaria has proven to be one of the deadliest and has exerted the most potent selective pressures on its target cell, the red blood cell. Red blood cells have recently gained recognition for their immunomodulatory properties, yet how red cell adaptations contribute to the host response during critical illness remains understudied. This review will discuss how adaptations that may have been advantageous for host survival might influence immune responses in modern critical illness. We will highlight the current evidence for divergent host resilience arising from the adaptations to malaria and summarize how understanding evolutionary red cell adaptations to malaria may provide insight into the heterogeneity of the host response to critical illness, perhaps driving future precision medicine approaches to syndromes affecting the critically ill such as sepsis and acute respiratory distress syndrome (ARDS).
MeSH term(s)	Humans ; Critical Illness ; Malaria ; Sepsis ; Erythrocytes ; Respiratory Distress Syndrome ; Immunity
Language	English
Publishing date	2023-01-03
Publishing country	United States
Document type	Review ; Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00127.2022
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Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: ExRNA Takes a Toll in Sepsis-associated Lung Injury.

Lam, L K Metthew / Mangalmurti, Nilam S

American journal of respiratory cell and molecular biology

2022 Volume 67, Issue 3, Page(s) 271–272

MeSH term(s)	Humans ; Lung Injury ; MicroRNAs ; Respiratory Distress Syndrome ; Sepsis/complications ; Toll-Like Receptor 7/genetics
Chemical Substances	MicroRNAs ; TLR7 protein, human ; Toll-Like Receptor 7
Language	English
Publishing date	2022-09-15
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2022-0237ED
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Article ; Online: Red Blood Cells Function as Reservoirs of Tumor DNA.

Thompson, Jeffrey C / Li, Sue / Jose, Joshua S / Predina, Jarrod / Gupta, Aasha / Eruslanov, Evgeniy / Singhal, Sunil / Albelda, Steven M / Mangalmurti, Nilam S

American journal of physiology. Lung cellular and molecular physiology

2024

Abstract: Novel screening techniques for early detection of lung cancer are urgently needed. Profiling circulating tumor cell-free DNA (ctDNA) has emerged as a promising tool for biopsy-free tumor genotyping. However, both the scarcity and short half-life of ctDNA ...

Abstract	Novel screening techniques for early detection of lung cancer are urgently needed. Profiling circulating tumor cell-free DNA (ctDNA) has emerged as a promising tool for biopsy-free tumor genotyping. However, both the scarcity and short half-life of ctDNA substantially limit the sensitivity and clinical utility of ctDNA detection methodologies. Our discovery that Red Blood Cells (RBCs) sequester mitochondrial DNA opens a new avenue for detecting circulating nucleic acids, as RBCs represent an unrecognized reservoir of circulating nucleic acid. Here, we show that RBCs acquire tumor DNA following co-culture with lung cancer cell lines harboring KRAS and EGFR mutations. RBC-bound tumor DNA is detectable in patients with early-stage Non-Small Cell Lung Cancer (NSCLC) but not in healthy controls by qPCR. Our results collectively uncover a previously unrecognized yet easily accessible reservoir of tumor DNA, offering a promising foundation for future RBC-based tumor diagnostics.
Language	English
Publishing date	2024-03-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00049.2024
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Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Collateral damage: necroptosis in the development of lung injury.

Faust, Hilary / Mangalmurti, Nilam S

American journal of physiology. Lung cellular and molecular physiology

2019 Volume 318, Issue 2, Page(s) L215–L225

Abstract: Cell death is increasingly recognized as a driving factor in the development of acute lung injury. Necroptosis, an immunogenic regulated cell death program important in innate immunity, has been implicated in the development of lung injury in a diverse ... ...

Abstract	Cell death is increasingly recognized as a driving factor in the development of acute lung injury. Necroptosis, an immunogenic regulated cell death program important in innate immunity, has been implicated in the development of lung injury in a diverse range of conditions. Characterized by lytic cell death and consequent extracellular release of endogenous inflammatory mediators, necroptosis can be both beneficial and deleterious to the host, depending on the context. Here, we review recent investigations linking necroptosis and the development of experimental lung injury. We assess the consequences of necroptosis during bacterial pneumonia, viral infection, sepsis, and sterile injury, highlighting increasing evidence from in vitro studies, animal models, and clinical studies that implicates necroptosis in the pathogenesis of ARDS. Lastly, we highlight current challenges in translating laboratory findings to the bedside.
MeSH term(s)	Animals ; Disease Models, Animal ; Humans ; Lung Injury/microbiology ; Lung Injury/pathology ; Lung Injury/virology ; Models, Biological ; Necroptosis ; Respiratory Tract Infections/complications ; Respiratory Tract Infections/microbiology ; Respiratory Tract Infections/virology
Language	English
Publishing date	2019-11-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00065.2019
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Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Inflammatory and tissue injury marker dynamics in pediatric acute respiratory distress syndrome.

Yehya, Nadir / Booth, Thomas J / Ardhanari, Gnana D / Thompson, Jill M / Lam, L K Metthew / Till, Jacob E / Mai, Mark V / Keim, Garrett / McKeone, Daniel J / Halstead, E Scott / Lahni, Patrick / Varisco, Brian M / Zhou, Wanding / Carpenter, Erica L / Christie, Jason D / Mangalmurti, Nilam S

The Journal of clinical investigation

2024

Abstract: Background: The molecular signature of pediatric acute respiratory distress syndrome (ARDS) is poorly described, and the degree to which hyperinflammation or specific tissue injury contributes to outcomes is unknown. Therefore, we profiled inflammation ... ...

Abstract	Background: The molecular signature of pediatric acute respiratory distress syndrome (ARDS) is poorly described, and the degree to which hyperinflammation or specific tissue injury contributes to outcomes is unknown. Therefore, we profiled inflammation and tissue injury dynamics over the first 7 days of ARDS, and associated specific biomarkers with mortality, persistent ARDS, and persistent multiple organ dysfunction syndrome (MODS). Methods: In a single-center prospective cohort of intubated pediatric ARDS, we collected plasma on days 0, 3, and 7. Nineteen biomarkers reflecting inflammation, tissue injury, and damage associated molecular patterns were measured. We assessed the relationship between biomarkers and trajectories with mortality, persistent ARDS, or persistent MODS using multivariable mixed effect models. Results: In 279 subjects (64 [23%] non-survivors), hyperinflammatory cytokines, tissue injury markers, and DAMPs were higher in non-survivors. Survivors and non-survivors showed different biomarker trajectories. IL-1α, sTNFR1, ANG2, and SPD increased in non-survivors, while DAMPs remained persistently elevated. ANG2 and P3NP were associated with persistent ARDS, whereas multiple cytokines, tissue injury markers, and DAMPs were associated with persistent MODS. Corticosteroid use did not impact the association of biomarker levels or trajectory with mortality. Conclusions: Pediatric ARDS survivors and non-survivors had distinct biomarker trajectories, with cytokines, endothelial and alveolar epithelial injury, and DAMPs elevated in non-survivors. Mortality markers overlapped with markers associated with persistent MODS, rather than persistent ARDS.
Language	English
Publishing date	2024-04-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI177896
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Article ; Online: The Evolving Erythrocyte: Red Blood Cells as Modulators of Innate Immunity.

Anderson, H Luke / Brodsky, Igor E / Mangalmurti, Nilam S

Journal of immunology (Baltimore, Md. : 1950)

2018 Volume 201, Issue 5, Page(s) 1343–1351

Abstract: The field of red cell biology is undergoing a quiet revolution. Long assumed to be inert oxygen carriers, RBCs are emerging as important modulators of the innate immune response. Erythrocytes bind and scavenge chemokines, nucleic acids, and pathogens in ... ...

Abstract	The field of red cell biology is undergoing a quiet revolution. Long assumed to be inert oxygen carriers, RBCs are emerging as important modulators of the innate immune response. Erythrocytes bind and scavenge chemokines, nucleic acids, and pathogens in circulation. Depending on the conditions of the microenvironment, erythrocytes may either promote immune activation or maintain immune quiescence. We examine erythrocyte immune function through a comparative and evolutionary lens, as this framework may offer perspective into newly recognized roles of human RBCs. Next, we review the known immune roles of human RBCs and discuss their activity in the context of sepsis where erythrocyte function may prove important to disease pathogenesis. Given the limited success of immunomodulatory therapies in treating inflammatory diseases, we propose that the immunologic function of RBCs provides an understudied and potentially rich area of research that may yield novel insights into mechanisms of immune regulation.
MeSH term(s)	Animals ; Biological Evolution ; Erythrocytes/immunology ; Humans ; Immunity, Innate ; Immunomodulation ; Sepsis/immunology ; Sepsis/pathology
Language	English
Publishing date	2018-08-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1800565
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Article: Neutrophil extracellular trap stabilization by platelet factor 4 reduces thrombogenicity and endothelial cell injury.

Ngo, Anh T P / Sarkar, Amrita / Yarovoi, Irene / Levine, Nate D / Bochenek, Veronica / Zhao, Guohua / Rauova, Lubica / Kowalska, M Anna / Eckart, Kaitlyn / Mangalmurti, Nilam S / Rux, Ann / Cines, Douglas B / Poncz, Mortimer / Gollomp, Kandace

bioRxiv : the preprint server for biology

2023

Abstract: Neutrophil extracellular traps (NETs) are abundant in sepsis, and proposed NET-directed therapies in sepsis prevent their formation or accelerate degradation. Yet NETs are important for microbial entrapment, as NET digestion liberates pathogens and NET ... ...

Abstract	Neutrophil extracellular traps (NETs) are abundant in sepsis, and proposed NET-directed therapies in sepsis prevent their formation or accelerate degradation. Yet NETs are important for microbial entrapment, as NET digestion liberates pathogens and NET degradation products (NDPs) that deleteriously promote thrombosis and endothelial cell injury. We proposed an alternative strategy of NET-stabilization with the chemokine, platelet factor 4 (PF4, CXCL4), which we have shown enhances NET-mediated microbial entrapment. We now show that NET compaction by PF4 reduces their thrombogenicity. In vitro, we quantified plasma thrombin and fibrin generation by intact or degraded NETs and cell-free (cf) DNA fragments, and found that digested NETs and short DNA fragments were more thrombogenic than intact NETs and high molecular weight genomic DNA, respectively. PF4 reduced the thrombogenicity of digested NETs and DNA by interfering, in part, with contact pathway activation. In endothelial cell culture studies, short DNA fragments promoted von Willebrand factor release and tissue factor expression via a toll-like receptor 9-dependent mechanism. PF4 blocked these effects. C
Language	English
Publishing date	2023-01-09
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.09.522931
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Article ; Online: RAGE interacts with the necroptotic protein RIPK3 and mediates transfusion-induced danger signal release.

Faust, Hilary / Lam, Lk Metthew / Hotz, Meghan J / Qing, Danielle / Mangalmurti, Nilam S

Vox sanguinis

2020 Volume 115, Issue 8, Page(s) 729–734

Abstract: RBC transfusion is associated with increased morbidity and mortality in critically ill patients. Endothelial cell necroptosis and subsequent damage-associated molecular pattern (DAMP) release has been identified as a mechanism of injury following RBC ... ...

Abstract	RBC transfusion is associated with increased morbidity and mortality in critically ill patients. Endothelial cell necroptosis and subsequent damage-associated molecular pattern (DAMP) release has been identified as a mechanism of injury following RBC transfusion. Mounting evidence implicates the pro-inflammatory pattern recognition receptor, Receptor for Advanced Glycation End Products (RAGE), in initiating cell death programmes such as necroptosis. Here, we demonstrate the role of RAGE in endothelial necroptosis, as deletion of RAGE attenuates necroptotic cell death in response to TNFα, LPS or CpG-DNA. We show direct interaction of RAGE with the critical mediator of necroptosis, Receptor Interacting Protein Kinase 3 (RIPK3), during necroptosis. Furthermore, we observe decreased plasma High Mobility Group Box 1 (HMGB1) and RIPK3 levels in RAGE deficient mice compared to WT mice post-transfusion, substantiating the role for RAGE in transfusion-induced DAMP release in vivo. Collectively, these findings underscore RAGE as an essential mediator of regulated necrosis and post-transfusion DAMP release. Further studies to understand the role of RAGE and the necroptotic pathway in transfusion-induced organ injury may offer key targets to mitigate transfusion-related risks, including the risk of ARDS, in susceptible hosts.
MeSH term(s)	Animals ; Endothelial Cells/physiology ; Erythrocyte Transfusion/adverse effects ; Female ; HMGB1 Protein ; Mice ; Mice, Inbred C57BL ; Necrosis/etiology ; Necrosis/metabolism ; Receptor for Advanced Glycation End Products/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	HMGB1 Protein ; Receptor for Advanced Glycation End Products ; Tumor Necrosis Factor-alpha ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk3 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2020-07-07
Publishing country	England
Document type	Journal Article
ZDB-ID	80313-3
ISSN	1423-0410 ; 0042-9007
ISSN (online)	1423-0410
ISSN	0042-9007
DOI	10.1111/vox.12946
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Article ; Online: Trefoil Factor Family: A Troika for Lung Repair and Regeneration.

Rossi, Heather L / Ortiz-Carpena, Jorge F / Tucker, Devon / Vaughan, Andrew E / Mangalmurti, Nilam S / Cohen, Noam A / Herbert, De'Broski R

American journal of respiratory cell and molecular biology

2021 Volume 66, Issue 3, Page(s) 252–259

Abstract: Tissue damage in the upper and lower airways caused by mechanical abrasion, noxious chemicals, or pathogenic organisms must be followed by rapid restorative processes; otherwise, persistent immunopathology and disease may ensue. This review will discuss ... ...

Abstract	Tissue damage in the upper and lower airways caused by mechanical abrasion, noxious chemicals, or pathogenic organisms must be followed by rapid restorative processes; otherwise, persistent immunopathology and disease may ensue. This review will discuss evidence for the important role served by trefoil factor (TFF) family members in healthy and diseased airways of humans and rodents. Collectively, these peptides serve to both maintain and restore homeostasis through their regulation of the mucous layer and their control of cell motility, cell differentiation, and immune function in the upper and lower airways. We will also discuss important differences in which trefoil member tracks with homeostasis and disease between humans and mice, which poses a challenge for research in this area. Moreover, we discuss new evidence supporting newly identified receptor binding partners in the leucine-rich repeat and immunoglobulin-like domain-containing NoGo (LINGO) family in mediating the biological effects of TFF proteins in mouse models of epithelial repair and infection. Recent advances in our knowledge regarding TFF peptides suggest that they may be reasonable therapeutic targets in the treatment of upper and lower airway diseases of diverse etiologies. Further work understanding their role in airway homeostasis, repair, and inflammation will benefit from these newly uncovered receptor-ligand interactions.
MeSH term(s)	Animals ; Lung/metabolism ; Mice ; Peptides/metabolism ; Proteins ; Trefoil Factor-2 ; Trefoil Factors
Chemical Substances	Peptides ; Proteins ; Trefoil Factor-2 ; Trefoil Factors
Language	English
Publishing date	2021-11-16
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2021-0373TR
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