Role of Neutrophil Extracellular Traps and Vesicles in Regulating Vascular Endothelial Permeability

Ma, Yonggang; Yang, Xiaoyuan; Chatterjee, Victor; Meegan, Jamie E.; Beard, Richard S.; Yuan, Sarah Y.

doi:10.3389/fimmu.2019.01037

Cited by 87 publications

(97 citation statements)

References 120 publications

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“…Likewise, I/R significantly elevated lung MPO levels, an effect attenuated by MLDL ( Figure 2B). Trans-endothelial migration of neutrophils involves the opening of endothelial barrier, causing increased permeability (2). Lung microvascular permeability, evaluated by Evans blue extravasation, was markedly elevated after gut I/R, and this effect was ameliorated by MLDL ( Figure 2C).…”

Section: Mldl Attenuates Intestinal I/r-induced Neutrophil Infiltratimentioning

confidence: 99%

“…During the process of neutrophil diapedesis, CD11b on neutrophil surface is upregulated and binds to endothelial adhesion molecules to form firm adhesion (2). We treated normal mouse whole blood with pre-I/R or post-I/R lymph, and measured neutrophil CD11b expression using multicolor flow cytometry.…”

Section: Post-i/r Lymph But Not Pre-i/r Lymph Increases Neutrophil mentioning

confidence: 99%

“…For example, trauma or sepsis is often associated with intestinal ischemia/reperfusion (I/R) injury, which results in gut barrier dysfunction and translocation of bacteria or injurious factors to the systemic circulation and remote tissues, further exacerbating organ dysfunction (1). Neutrophil activation and infiltration into the lungs are a hallmark of ALI, where activated neutrophils cause tissue damage through multiple mechanisms, including secreting pro-inflammatory mediators (2,3). However, the underlying mechanisms by which gut I/R leads to lung neutrophil infiltration and activation are incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

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Gut Ischemia Reperfusion Injury Induces Lung Inflammation via Mesenteric Lymph-Mediated Neutrophil Activation

Zabell

Creasy

et al. 2020

Front. Immunol.

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Gut ischemia/reperfusion (I/R) injury is a common clinical problem associated with significant mortality and morbidities that result from systemic inflammation and remote organ dysfunction, typically acute lung injury. The mechanisms underlying the dissemination of gut-derived harmful mediators into the circulation are poorly understood. The objective of our study was to determine the role of mesenteric lymphatic circulation in the systemic and pulmonary inflammatory response to gut I/R. Using a murine intestinal I/R model, we evaluated whether and how blocking mesenteric lymph flow affects the inflammatory response in local tissues (gut) and remote organs (lungs). We further explored the mechanisms of post-I/R lymph-induced systemic inflammation by examining neutrophil activity and interaction with endothelial cells in vitro. Mice subjected to intestinal I/R displayed a significant inflammatory response in local tissues, evidenced by neutrophil infiltration into mucosal areas, as well as lung inflammation, evidenced by increased myeloperoxidase levels, neutrophil infiltration, and elevated microvascular permeability in the lungs. Mesenteric lymph duct ligation (MLDL) had no effect on gut injury per se, but effectively attenuated lung injury following gut I/R. Cell experiments showed that lymph fluid from post-I/R animals, but not pre-I/R, increased neutrophil surface CD11b expression and their ability to migrate across vascular endothelial monolayers. Moreover, post-I/R lymph upregulated neutrophil expression of pro-inflammatory cytokines and chemokines, which was mediated by a mechanism involving nuclear factor (NF)-κB signaling. Consistently, gut I/R activated NF-κB in lung neutrophils, which was alleviated by MLDL. In conclusion, all these data indicate that mesenteric lymph circulation contributes to neutrophil activation and lung inflammation following gut I/R injury partly through activating NF-κB.

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Section: Mldl Attenuates Intestinal I/r-induced Neutrophil Infiltratimentioning

confidence: 99%

Section: Post-i/r Lymph But Not Pre-i/r Lymph Increases Neutrophil mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Gut Ischemia Reperfusion Injury Induces Lung Inflammation via Mesenteric Lymph-Mediated Neutrophil Activation

Zabell

Creasy

et al. 2020

Front. Immunol.

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“…During the ARDS process, activated neutrophils release intracellular toxic components so as to amplify the inflammatory response by recruiting more inflammatory cells into the site of damage [34]. Additionally, Ma et al [35] reported that neutrophils were involved in regulating the microvascular endothelial permeability. Suzuki et al [36] reported that neutrophil elastase damaged the pulmonary endothelial glycocalyx in LPS-induced endotoxemia.…”

Section: Figmentioning

confidence: 99%

Crocin alleviates lipopolysaccharide-induced acute respiratory distress syndrome by protecting against glycocalyx damage and suppressing inflammatory signaling pathways

Zhang

Zhu

et al. 2020

Inflamm. Res.

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Objective To explore the mechanisms of crocin against glycocalyx damage and inflammatory injury in lipopolysaccharide (LPS)-induced acute respiratory distress syndrome (ARDS) mice and LPS-stimulated human umbilical vein endothelial cells (HUVECs). Methods Mice were randomly divided into control, LPS, and crocin + LPS (15, 30, and 60 mg/kg) groups. HUVECs were separated into eight groups: control, crocin, matrix metalloproteinase 9 inhibitor (MMP-9 inhib), cathepsin L inhibitor (CTL inhib), LPS, MMP-9 inhib + LPS, CTL inhib + LPS, and crocin + LPS. The potential cytotoxic effect of crocin on HUVECs was mainly evaluated through methylthiazolyldiphenyl-tetrazolium bromide assay. Histological changes were assessed via hemotoxylin and eosin staining. Lung capillary permeability was detected on the basis of wet-dry ratio and through fluorescein isothiocyanate-albumin assay. Then, protein levels were detected through Western blot analysis, immunohistochemical staining, and immunofluorescence. Results This study showed that crocin can improve the pulmonary vascular permeability in mice with LPS-induced ARDS and inhibit the inflammatory signaling pathways of high mobility group box, nuclear factor κB, and mitogen-activated protein kinase in vivo and in vitro. Crocin also protected against the degradation of endothelial glycocalyx heparan sulfate and syndecan-4 by inhibiting the expressions of CTL, heparanase, and MMP-9 in vivo and in vitro. Overall, this study revealed the protective effects of crocin on LPS-induced ARDS and elaborated their underlying mechanism. Conclusion Crocin alleviated LPS-induced ARDS by protecting against glycocalyx damage and suppressing inflammatory signaling pathways.Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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“…Mast cells are implicated especially as a source of histamine. There is interest in neutrophil products and especially in the possibility that these cells participate in more sustained plasma leaks [70, 71]. Once extravasated, additional plasma-derived players, typically kininogen-produced bradykinin [72, 73], may contribute.…”

Section: Plasma Exudation and Exudative Hyperresponsiveness At Viral mentioning

confidence: 99%

Humoral First-Line Mucosal Innate Defence in vivo

Persson¹

2020

J Innate Immun

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Based on observations in vivo in guinea-pig and human airways, this review presents plasma exudation as non-sieved transmission of bulk plasma across an unperturbed mucosa that maintains its normal barrier functions. Several steps have led to the present understanding of plasma exudation as a non-injurious response to mucosal challenges. The implication of a swift appearance of all circulating multipotent protein systems (also including antimicrobial peptides that now are viewed as being exclusively produced by local cells) on challenged, but intact, mucosal surfaces cannot be trivial. Yet, involvement of early plasma exudation responses in innate mucosal immunology has dwelled below the radar. Admittedly, exploration of physiological plasma exudation mechanisms requires in vivo approaches beyond mouse studies. Plasma exudation also lacks the specificity that is a hallmark of biological revelations. These aspects separate plasma exudation from mainstream progress in immunology. The whole idea, presented here, thus competes with strong paradigms currently entertained in the accepted research front. The present focus on humoral innate immunity in vivo further deviates from most discussions, which concern cell-mediated innate defence. Indeed, plasma exudation has emerged as sole in vivo source of major mucosal defence proteins that now are viewed as local cell produce. In conclusion, this review highlights opportunities for complex actions and interactions provided by non-sieved plasma proteins/peptides on the surface of intact mucosal barriers in vivo.

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Role of Neutrophil Extracellular Traps and Vesicles in Regulating Vascular Endothelial Permeability

Cited by 87 publications

References 120 publications

Gut Ischemia Reperfusion Injury Induces Lung Inflammation via Mesenteric Lymph-Mediated Neutrophil Activation

Gut Ischemia Reperfusion Injury Induces Lung Inflammation via Mesenteric Lymph-Mediated Neutrophil Activation

Crocin alleviates lipopolysaccharide-induced acute respiratory distress syndrome by protecting against glycocalyx damage and suppressing inflammatory signaling pathways

Humoral First-Line Mucosal Innate Defence in vivo

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