Current Understanding on the Metabolism of Neutrophils

Jeon, Jae‐Han; Hong, Chang-Won; Kim, Eun Young; Lee, Jae Man

doi:10.4110/in.2020.20.e46

Cited by 59 publications

(64 citation statements)

References 69 publications

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“…This can be partially attributed to their immune origin wherein processes like degranulation also contribute to glycolysis, exocytosis, and the production of cell energy [83]. In light of their potent enrichment in glycolytic pathways, we chose to focus on aspects related to EV-mediated mitochondrial transfer for the remainder of this study.…”

Section: Gene Ontology and Pathway Enrichment Analysesmentioning

confidence: 99%

Microvesicles Transfer Mitochondria and Increase Mitochondrial Function in Brain Endothelial Cells

D’Souza

Burch

Dave

et al. 2021

Preprint

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Extracellular vesicles (EVs) such as exosomes (EXOs) and microvesicles (MVs) are promising carriers for the delivery of biologic drugs such as nucleic acids and proteins. We have demonstrated, for the first time, that EVs derived from hCMEC/D3: a human brain endothelial cell (BEC) line transfer polarized mitochondria to recipient BECs in culture and to neurons in mice acute brain cortical and hippocampal slices. This mitochondrial transfer increased ATP levels by 100 to 200-fold (relative to untreated cells) in the recipient BECs exposed to oxygen-glucose deprivation, an in vitro model of cerebral ischemia. Our previous studies suggested that EXOs, the smaller vesicle subpopulation, derived from a macrophage cell line (RAW264.7) load more exogenous plasmid DNA compared to the larger MVs and the RAW-derived EXOs also demonstrated greater transfection in the recipient BECs compared to EXOs derived from the homotypic hCMEC/D3 BECs. Proteomic analysis of EVs indicated that RAW-EVs are preferentially enriched with proteins that are involved in the trafficking of DNA-containing particles from the cytoplasm towards the nucleus. Intriguingly, although the heterotypic macrophage-derived EVs demonstrated increased transfection in the recipient BECs; the homotypic, BEC-derived EVs demonstrated a greater selectivity to transfer polarized mitochondria and increase endothelial cell survival under ischemic conditions.

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Section: Gene Ontology and Pathway Enrichment Analysesmentioning

confidence: 99%

Microvesicles Transfer Mitochondria and Increase Mitochondrial Function in Brain Endothelial Cells

D’Souza

Burch

Dave

et al. 2021

Preprint

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“…Neutrophils have only a few mitochondria, and consequently, at rest, consume only small amounts of O 2 . Upon activation—that is, with initiation of chemotaxis and phagocytosis [ 135 ]—ATP turnover remains mostly unaffected [ 136 , 137 ], whereas O 2 requirements markedly increase due to the respiratory burst. Glycolysis is crucial for phagocytosis and the formation of neutrophil extracellular traps (NETs) [ 65 , 138 ].…”

Section: Immuno-metabolismmentioning

confidence: 99%

Energetic dysfunction in sepsis: a narrative review

Preau

Vodovar

Jung

et al. 2021

Ann. Intensive Care

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Background Growing evidence associates organ dysfunction(s) with impaired metabolism in sepsis. Recent research has increased our understanding of the role of substrate utilization and mitochondrial dysfunction in the pathophysiology of sepsis-related organ dysfunction. The purpose of this review is to present this evidence as a coherent whole and to highlight future research directions. Main text Sepsis is characterized by systemic and organ-specific changes in metabolism. Alterations of oxygen consumption, increased levels of circulating substrates, impaired glucose and lipid oxidation, and mitochondrial dysfunction are all associated with organ dysfunction and poor outcomes in both animal models and patients. The pathophysiological relevance of bioenergetics and metabolism in the specific examples of sepsis-related immunodeficiency, cerebral dysfunction, cardiomyopathy, acute kidney injury and diaphragmatic failure is also described. Conclusions Recent understandings in substrate utilization and mitochondrial dysfunction may pave the way for new diagnostic and therapeutic approaches. These findings could help physicians to identify distinct subgroups of sepsis and to develop personalized treatment strategies. Implications for their use as bioenergetic targets to identify metabolism- and mitochondria-targeted treatments need to be evaluated in future studies.

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“…All the REACTOME-identified proteins engaged in neutrophil degranulation and also in other innate and adaptive immune processes, regardless of their S -palmitoylation status, found after 4 and 12 weeks of feeding are collected in Supplemental Table S3 (sheet 5), while those whose S -palmitoylation was most strongly affected by the HPD diet are shown in Table 1 . It can be seen that among such proteins was starch-binding domain-containing protein 1 ( Stbd1 ) which contributes to glycogen catabolism, in agreement with glycolysis as the main energy source of activated neutrophils [ 41 ]. Table 1 shows that S -palmitoylated proteins involved in neutrophil degranulation were affected by the HPD diet either at the protein or S -palmitoylation level, or both.…”

Section: Resultsmentioning

confidence: 99%

Palm Oil-Rich Diet Affects Murine Liver Proteome and S-Palmitoylome

Ziemlińska

Sobocińska

Świątkowska

et al. 2021

IJMS

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Palmitic acid (C16:0) is the most abundant saturated fatty acid in animals serving as a substrate in synthesis and β-oxidation of other lipids, and in the modification of proteins called palmitoylation. The influence of dietary palmitic acid on protein S-palmitoylation remains largely unknown. In this study we performed high-throughput proteomic analyses of a membrane-enriched fraction of murine liver to examine the influence of a palm oil-rich diet (HPD) on S-palmitoylation of proteins. HPD feeding for 4 weeks led to an accumulation of C16:0 and C18:1 fatty acids in livers which disappeared after 12-week feeding, in contrast to an accumulation of C16:0 in peritoneal macrophages. Parallel proteomic studies revealed that HPD feeding induced a sequence of changes of the level and/or S-palmitoylation of diverse liver proteins involved in fatty acid, cholesterol and amino acid metabolism, hemostasis, and neutrophil degranulation. The HPD diet did not lead to liver damage, however, it caused progressing obesity, hypercholesterolemia and hyperglycemia. We conclude that the relatively mild negative impact of such diet on liver functioning can be attributed to a lower bioavailability of palm oil-derived C16:0 vs. that of C18:1 and the efficiency of mechanisms preventing liver injury, possibly including dynamic protein S-palmitoylation.

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Current Understanding on the Metabolism of Neutrophils

Cited by 59 publications

References 69 publications

Microvesicles Transfer Mitochondria and Increase Mitochondrial Function in Brain Endothelial Cells

Microvesicles Transfer Mitochondria and Increase Mitochondrial Function in Brain Endothelial Cells

Energetic dysfunction in sepsis: a narrative review

Palm Oil-Rich Diet Affects Murine Liver Proteome and S-Palmitoylome

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