Contemporary Lifestyle and Neutrophil Extracellular Traps: An Emerging Link in Atherosclerosis Disease

Pérez-Olivares, Laura; Soehnlein, Oliver

doi:10.3390/cells10081985

Cited by 11 publications

(10 citation statements)

References 251 publications

(312 reference statements)

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“…As Fig. 6 B shows, endothelial nitric oxide synthase (NOS3) levels were increased in Apoe −/− mice treated with iE-DAP, in agreement with the effect of NO on the regulation of atherogenesis and NETosis [ 48 , 49 ]; however, the interplay of all of these issues with NOD1 activation has not been investigated before. Moreover, an increase in P-p65, P-ERK and P-p38 and mainly in H3Cit.…”

Section: Resultssupporting

confidence: 58%

High-fat diet activates splenic NOD1 and enhances neutrophil recruitment and neutrophil extracellular traps release in the spleen of ApoE-deficient mice

Fernández-García

González-Ramos

Avendaño-Ortíz

et al. 2022

Cell. Mol. Life Sci.

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In the course of atherogenesis, the spleen plays an important role in the regulation of extramedullary hematopoiesis, and in the control of circulating immune cells, which contributes to plaque progression. Here, we have investigated the role of splenic nucleotide-binding oligomerization domain 1 (NOD1) in the recruitment of circulating immune cells, as well as the involvement of this immune organ in extramedullary hematopoiesis in mice fed on a high-fat high-cholesterol diet (HFD). Under HFD conditions, the absence of NOD1 enhances the mobilization of immune cells, mainly neutrophils, from the bone marrow to the blood. To determine the effect of NOD1-dependent mobilization of immune cells under pro-atherogenic conditions, Apoe−/− and Apoe−/−Nod1−/− mice fed on HFD for 4 weeks were used. Splenic NOD1 from Apoe−/− mice was activated after feeding HFD as inferred by the phosphorylation of the NOD1 downstream targets RIPK2 and TAK1. Moreover, this activation was accompanied by the release of neutrophil extracellular traps (NETs), as determined by the increase in the expression of peptidyl arginine deiminase 4, and the identification of citrullinated histone H3 in this organ. This formation of NETs was significantly reduced in Apoe−/−Nod1−/− mice. Indeed, the presence of Ly6G+ cells and the lipidic content in the spleen of mice deficient in Apoe and Nod1 was reduced when compared to the Apoe−/− counterparts, which suggests that the mobilization and activation of circulating immune cells are altered in the absence of NOD1. Furthermore, confirming previous studies, Apoe−/−Nod1−/− mice showed a reduced atherogenic disease, and diminished recruitment of neutrophils in the spleen, compared to Apoe−/− mice. However, splenic artery ligation reduced the atherogenic burden in Apoe−/− mice an effect that, unexpectedly was lost in Apoe−/−Nod1−/− mice. Together, these results suggest that neutrophil accumulation and activity in the spleen are driven in part by NOD1 activation in mice fed on HFD, contributing in this way to regulating atherogenic progression.

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Section: Resultssupporting

confidence: 58%

High-fat diet activates splenic NOD1 and enhances neutrophil recruitment and neutrophil extracellular traps release in the spleen of ApoE-deficient mice

Fernández-García

González-Ramos

Avendaño-Ortíz

et al. 2022

Cell. Mol. Life Sci.

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“…Smoking has been reported to strongly affect the function of neutrophils, e.g., chemotaxis, phagocytosis, and inflammatory response [ 10 ]. Increased NET formation is described in smokers with chronic obstructive pulmonary disease, thrombosis, or atherosclerosis [ 11 , 12 ], but has not yet been associated with impaired wound healing.…”

Section: Introductionmentioning

confidence: 99%

Nicotine and Cotinine Induce Neutrophil Extracellular Trap Formation—Potential Risk for Impaired Wound Healing in Smokers

Aspera-Werz¹,

Mück²,

Herbst³

et al. 2022

Antioxidants

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Smoking undoubtedly affects human health. Investigating 2318 representative patients at a level 1 trauma center identified delayed wound healing, tissue infections, and/or sepsis as main complications in smokers following trauma and orthopedic surgery. Therefore, smoking cessation is strongly advised to improve the clinical outcome in these patients, although smoking cessation often fails despite nicotine replacement therapy raising the need for specific interventions that may reduce the complication rate. However, the underlying mechanisms are still unknown. In diabetics, delayed wound healing and infections/sepsis are associated with increased neutrophilic PADI4 expression and formation of neutrophil extracellular traps (NETs). The aim was to investigate if similar mechanisms hold for smokers. Indeed, our results show higher PADI4 expression in active and heavy smokers than non-smokers, which is associated with an increased complication rate. However, in vitro stimulation of neutrophils with cigarette smoke extract (CSE) only moderately induced NET formation despite accumulation of reactive oxygen species (ROS). Physiological levels of nicotine and its main metabolite cotinine more effectively induced NET formation, although they did not actively induce the formation of ROS, but interfered with the activity of enzymes involved in anti-oxidative defense and NET formation. In summary, we propose increased formation of NETs as possible triggers for delayed wound healing, tissue infections, and/or sepsis in smokers after a major trauma and orthopedic surgery. Smoking cessation might reduce this effect. However, our data show that smoking cessation supported by nicotine replacement therapy should be carefully considered as nicotine and its metabolite cotinine effectively induced NET formation in vitro, even without active formation of ROS.

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“…NETs were originally described as a defense mechanism to entrap and kill invading microorganisms [ 15 ]. During the last decades, NETs have been implicated in various conditions such as cancer [ 16 , 17 , 18 , 19 ], cardiovascular diseases [ 20 , 21 , 22 ], and autoimmune [ 19 , 23 , 24 , 25 ] and respiratory disorders [ 26 ]. A growing body of literature has emerged exploring the relationship between NETs and chronic inflammatory airway diseases, including asthma [ 27 , 28 , 29 ] and chronic obstructive pulmonary disease (COPD) [ 30 ].…”

Section: Introductionmentioning

confidence: 99%

Neutrophil Extracellular Traps in Asthma: Friends or Foes?

Poto

Shamji

Marone

et al. 2022

Cells

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Asthma is a chronic inflammatory disease characterized by variable airflow limitation and airway hyperresponsiveness. A plethora of immune and structural cells are involved in asthma pathogenesis. The roles of neutrophils and their mediators in different asthma phenotypes are largely unknown. Neutrophil extracellular traps (NETs) are net-like structures composed of DNA scaffolds, histones and granular proteins released by activated neutrophils. NETs were originally described as a process to entrap and kill a variety of microorganisms. NET formation can be achieved through a cell-death process, termed NETosis, or in association with the release of DNA from viable neutrophils. NETs can also promote the resolution of inflammation by degrading cytokines and chemokines. NETs have been implicated in the pathogenesis of various non-infectious conditions, including autoimmunity, cancer and even allergic disorders. Putative surrogate NET biomarkers (e.g., double-strand DNA (dsDNA), myeloperoxidase-DNA (MPO-DNA), and citrullinated histone H3 (CitH3)) have been found in different sites/fluids of patients with asthma. Targeting NETs has been proposed as a therapeutic strategy in several diseases. However, different NETs and NET components may have alternate, even opposite, consequences on inflammation. Here we review recent findings emphasizing the pathogenic and therapeutic potential of NETs in asthma.

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Contemporary Lifestyle and Neutrophil Extracellular Traps: An Emerging Link in Atherosclerosis Disease

Cited by 11 publications

References 251 publications

High-fat diet activates splenic NOD1 and enhances neutrophil recruitment and neutrophil extracellular traps release in the spleen of ApoE-deficient mice

High-fat diet activates splenic NOD1 and enhances neutrophil recruitment and neutrophil extracellular traps release in the spleen of ApoE-deficient mice

Nicotine and Cotinine Induce Neutrophil Extracellular Trap Formation—Potential Risk for Impaired Wound Healing in Smokers

Neutrophil Extracellular Traps in Asthma: Friends or Foes?

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