Autophagy Primes Neutrophils for Neutrophil Extracellular Trap Formation during Sepsis

Park, So Young; Shrestha, Sanjeeb; Youn, Young-Jin; Kim, Jun-Kyu; Kim, Shin-Yeong; Kim, Hyun Jung; Park, Sohee; Ahn, Won-Gyun; Kim, Shin; Lee, Myung Goo; Jung, Ki‐Suck; Park, Yong Bum; Mo, Eun-Kyung; Ko, Yousang; Lee, Suh-Young; Koh, Younsuck; Park, Myung Jae; Song, Dong‐Keun; Hong, Chang-Won

doi:10.1164/rccm.201603-0596oc

Cited by 119 publications

(107 citation statements)

References 52 publications

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“…The observation that corticosteroids lead to a prolonged lower level of NETs in recovering patients who have a better outcome does perhaps suggest a beneficial role for NETosis during the process of recovering from pneumonia, and would be in keeping with other recent data suggesting that patients who survive sepsis may indeed have a greater ability to make NETs than non-survivors [24]. Recent data from CF patients has suggested that a delay in neutrophil apoptosis in these subjects leads to an increased ability to form NETs [21], suggesting that the activation of alternative routes of disposal for neutrophils may have consequences in terms of promoting inflammation.…”

supporting

confidence: 84%

NETs in pneumonia: is just enough the right amount?

Gray

2018

Eur Respir J

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supporting

confidence: 84%

NETs in pneumonia: is just enough the right amount?

Gray

2018

Eur Respir J

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“…Because the phagocytic cells are encountered with pathogens, dysregulated immune response (Bangsgaard, Hjorth, Olufsen, Mehlsen, & Ottesen, ) cause to the release of products such as chemokines, cytokine, lipid mediators, nitric oxide (NO), and oxygen radicals (Arango Duque & Descoteaux, ; Markose, Kirkland, Ramachandran, & Henderson, ). On the other hand, the activation of neutrophils increases the bacteria clearance and causes inflammation and tissue damage (Park et al, ) through respiratory burst (Bae et al, ), myeloperoxidases (MPOs; Schrijver, Kemperman, Roest, Kesecioglu, & de Lange, ), proteases, and releasing several cytokine mediators (Bosmann & Ward, ; Park et al, ). Neutrophils also release neutrophil extracellular traps that lead to increase vascular inflammation and coagulation (Martinod et al, ; McDonald et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…activation of neutrophils increases the bacteria clearance and causes inflammation and tissue damage (Park et al, 2017) through respiratory burst , myeloperoxidases (MPOs; Schrijver, Kemperman, Roest, Kesecioglu, & de Lange, 2017), proteases, and releasing several cytokine mediators (Bosmann & Ward, 2013;Park et al, 2017). Neutrophils also release neutrophil extracellular traps that lead to increase vascular inflammation and coagulation (Martinod et al, 2013;McDonald et al, 2017).…”

mentioning

confidence: 99%

Therapeutic effects of curcumin on sepsis and mechanisms of action: A systematic review of preclinical studies

Karimi

Ghodsi

Kooshki

et al. 2019

Phytotherapy Research

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Sepsis is a complex disease that begins with an infectious disorder and causes excessive immune responses. Curcumin is considered as an active component of turmeric that can improve the condition in sepsis due to its anti‐inflammatory and antioxidant properties. PubMed, Embase, Google Scholar, Web of Science, and Scopus databases were searched. Searching was not limited to a specific publication period. Only English‐language original articles, which had examined the effect of curcumin on sepsis, were included. At first, 1,098 articles were totally found, and 209 articles were selected after excluding duplicated data; 46 articles were remained due to the curcumin effects on sepsis. These included 23 in vitro studies and 23 animal studies. Our results showed that curcumin and various analogs of curcumin can have an inhibitory effect on sepsis‐induced complications. Curcumin has the ability to inhibit the inflammatory, oxidative coagulation factors, and regulation of immune responses in sepsis. Despite the promising evidence of the therapeutic effects of curcumin on the sepsis complication, further studies seem necessary to investigate its effect and possible mechanisms of action in human studies.

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“…Because NDTRs and NDMVs exerted different effects on the phenotypic polarization of macrophages, we next evaluated the clinical implication of NDTRs and NDMVs in the murine models of acute and chronic inflammation. We employed an experimental sepsis model (cecalligation and puncture, CLP) to establish murine model of acute inflammation (Park et al, 2017) and a chronic dextran sulfate sodium (DSS)-induced colitis model to establish a murine model of chronic inflammation (Marcon et al, 2013). BALB/c mice were treated intraperitoneally with either NDTRs or NDMVs 30 min prior to CLP surgery and further treated on days 1, 2, and 3 after CLP surgery.…”

Section: Resultsmentioning

confidence: 99%

“…BALB/c (male, 5-8 weeks old) mice were purchased from Orient Bio. Mouse neutrophils were isolated from bone marrow of healthy mouse using neutrophil enrichment kit (Miltenyi Biotec) or EasySep™ mouse neutrophil enrichment kit (StemCell technologies) as previously described (Park et al, 2017). EVs were isolated from neutrophils stimulated with E. coli .…”

Section: Methodsmentioning

confidence: 99%

Neutrophil-derived extracellular vesicles: proinflammatory trails and anti-inflammatory microvesicles

Youn

Shrestha

et al. 2019

Preprint

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SUMMARYExtracellular vesicles (EVs) are membrane-derived vesicles that mediate intercellular communications. Neutrophils produce different subtypes of EVs during inflammatory responses. Neutrophil-derived trails (NDTRs) are generated by neutrophils migrating toward inflammatory foci, whereas neutrophil-derived microvesicles (NDMVs) are thought to be generated by neutrophils that have arrived at the inflammatory foci. However, the physical and functional characteristics of neutrophil-derived EVs are incompletely understood. In this study, we investigated the similarities and differences between neutrophil-derived EV subtypes. Neutrophil-derived EVs shared similar characteristics regarding stimulators, generation mechanisms, and surface marker expression. Both neutrophil-derived EV subtypes exhibited similar functions, such as direct bactericidal activity and induction of monocyte chemotaxis via MCP-1. However, NDTR generation was dependent on the integrin signaling, while NDMV generation was dependent on the PI3K pathway. The CD16 expression level differentiated the neutrophil-derived EV subtypes. Interestingly, both subtypes showed different patterns of miRNA expression and were easily phagocytosed by monocytes. NDTRs induced M1 macrophage polarization, whereas NDMVs induced M2 macrophage polarization. Moreover, NDTRs but not NDMVs exerted protective effects against sepsis-induced lethality in a murine sepsis model and pathological changes in a murine chronic colitis model. These results suggest a new insight into neutrophil-derived EV subtypes: proinflammatory NDTRs and anti-inflammatory NDMVs.Key pointsNeutrophil-derived trails are proinflammatory extracellular vesicles that induce M1 macrophage polarization and protect against inflammationNeutrophil-derived microvesicles are anti-inflammatory extracellular vesicles that induce M2 macrophage polarization

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Autophagy Primes Neutrophils for Neutrophil Extracellular Trap Formation during Sepsis

Abstract: These results indicate that neutrophil autophagy primes neutrophils for increased NET formation, which is important for proper neutrophil effector functions during sepsis. Our study provides important insights into the role of autophagy in neutrophils during sepsis.

Cited by 119 publications

References 52 publications

NETs in pneumonia: is just enough the right amount?

NETs in pneumonia: is just enough the right amount?

Therapeutic effects of curcumin on sepsis and mechanisms of action: A systematic review of preclinical studies

Neutrophil-derived extracellular vesicles: proinflammatory trails and anti-inflammatory microvesicles

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