Modulating inflammatory macrophages with an apoptotic body-inspired nanoparticle

Kraynak, Chelsea A.; Yan, Derek; Suggs, Laura J.

doi:10.1016/j.actbio.2020.03.041

Cited by 48 publications

(35 citation statements)

References 58 publications

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“…Among adults with type 2 diabetes, breaks in sitting with light-intensity walk or simple resistance activities (e.g., squats, calf raises) changed concentrations of 4 lipid classes and 37 lipid species (39). In this study, active breaks in siting only altered free fatty acids concentrations, whereas exercise modified 6 lipid classes and subclasses in a direction that suggests reduction in inflammation and platelet activation, and increase in antioxidant capacity, as presumed by the metabolic functions of these lipids (40)(41)(42)(43)(44). Of relevance, patients with rheumatoid arthritis were shown to have reduced alkenylphosphatidylethanolamine and phosphatidylserine, which are thought to contribute to higher cardiovascular risk and joint inflammation (45).…”

Section: Discussionmentioning

confidence: 56%

Acute cardiometabolic effects of brief active breaks in sitting for patients with rheumatoid arthritis

Pinto

Meireles

Peçanha

et al. 2021

American Journal of Physiology-Endocrinology and Metabolism

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Exercise is a treatment in rheumatoid arthritis but participation in moderate-to-vigorous exercise is challenging for some patients. Light-intensity breaks in sitting could be a promising alternative. We compared the acute effects of active breaks in sitting with those of moderate-to-vigorous exercise on cardiometabolic risk markers in patients with rheumatoid arthritis. In a cross-over fashion, 15 women with rheumatoid arthritis underwent three 8-h experimental conditions: prolonged sitting (SIT), 30-min bout of moderate-to-vigorous exercise followed by prolonged sitting (EX), and 3-min bout of light-intensity walking every 30 min of sitting (BR). Postprandial glucose, insulin, c-peptide, triglycerides, cytokines, lipid classes/subclasses (lipidomics), and blood pressure responses were assessed. Muscle biopsies were collected following each session to assess targeted proteins/genes. Glucose (-28% in area under the curve (AUC), p=0.036), insulin (-28% in AUC, p=0.016) and c-peptide (-27% in AUC, p=0.006) postprandial responses were attenuated in BR vs. SIT, whereas only c-peptide was lower in EX vs. SIT (-20% in AUC, p=0.002). IL-1β decreased during BR, but increased during EX and SIT (p=0.027 and p=0.085). IL-1ra was increased during EX vs. BR (p=0.002). TNF-α concentrations decreased during BR vs. EX (p=0.022). EX, but not BR, reduced systolic blood pressure (p=0.013). Lipidomic analysis showed that 7 of 36 lipid classes/subclasses were significantly different between conditions, with greater changes being observed in EX. No differences were observed for protein/gene expression. Brief active interruptions to sitting can offset markers of cardiometabolic disturbance, which may be particularly useful for patients who may find it difficult to adhere to exercise.

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Section: Discussionmentioning

confidence: 56%

Acute cardiometabolic effects of brief active breaks in sitting for patients with rheumatoid arthritis

Pinto

Meireles

Peçanha

et al. 2021

American Journal of Physiology-Endocrinology and Metabolism

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“…Priming M2 macrophages is a novel method to increase their efferocytosis to initiate the resolution phase of inflammation. In a previous study, nanoparticles were comprised of a poly(lactide-co-glycolide) as a core and a coating with phosphatidylserine (PS)-supplemented cell plasma membrane (PS-MNP) to mimic the apoptotic cell surface [137]. The macrophage engulfment of these nanoparticles elicited the polarization of M2 macrophages, and subsequently, inflammation was reduced via the NF-κB pathway.…”

Section: Controlling Cellular Phenotypesmentioning

confidence: 99%

Neutrophils and Macrophages as Targets for Development of Nanotherapeutics in Inflammatory Diseases

Gao

Kaur

et al. 2020

Pharmaceutics

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Neutrophils and macrophages are major components of innate systems, playing central roles in inflammation responses to infections and tissue injury. If they are out of control, inflammation responses can cause the pathogenesis of a wide range of diseases, such as inflammatory disorders and autoimmune diseases. Precisely regulating the functions of neutrophils and macrophages in vivo is a potential strategy to develop immunotherapies to treat inflammatory diseases. Advances in nanotechnology have enabled us to design nanoparticles capable of targeting neutrophils or macrophages in vivo. This review discusses the current status of how nanoparticles specifically target neutrophils or macrophages and how they manipulate leukocyte functions to inhibit their activation for inflammation resolution or to restore their defense ability for pathogen clearance. Finally, we present a novel concept of hijacking leukocytes to deliver nanotherapeutics across the blood vessel barrier. This review highlights the challenges and opportunities in developing nanotherapeutics to target leukocytes for improved treatment of inflammatory diseases.

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“…Some examples include an alginate-based nanoparticle system developed to deliver IL-10 plasmid DNA to repolarize M1 macrophages to M2 macrophages; 264 polyethylenimine nanoparticles used to deliver the gene for CD163, an M2 macrophage marker; 265 and PLGA nanoparticles used to mimic apoptotic bodies via a phospholipid membrane coating supplemented with phosphatidylserine to trigger the memory of uptake of apoptotic bodies, inducing an M2 polarization. 266 All of these strategies led to decreases in the release of inflammatory cytokines including IL-6, IL-1β, IFN-γ, TNF-α, and MCP-1 and led to the repolarization of macrophages toward the M2 phenotype. These materials and methods were used in vitro, but their resultant reduction in the release of inflammatory cytokines and macrophage repolarization indicates their potential to be used to reduce or eliminate the inflammation induced by macrophages during SARS-CoV-2 infection.…”

Section: Engineering Opportunities For Covid-19mentioning

confidence: 99%

“…A plethora of strategies has been developed to influence inflammatory macrophage response. Some examples include an alginate-based nanoparticle system developed to deliver IL-10 plasmid DNA to repolarize M1 macrophages to M2 macrophages; polyethylenimine nanoparticles used to deliver the gene for CD163, an M2 macrophage marker; and PLGA nanoparticles used to mimic apoptotic bodies via a phospholipid membrane coating supplemented with phosphatidylserine to trigger the memory of uptake of apoptotic bodies, inducing an M2 polarization . All of these strategies led to decreases in the release of inflammatory cytokines including IL-6, IL-1β, IFN-γ, TNF-α, and MCP-1 and led to the repolarization of macrophages toward the M2 phenotype.…”

Section: Biomaterials and Particle-based Immune Engineering Opportuni...mentioning

confidence: 99%

Biomaterials-Based Opportunities to Engineer the Pulmonary Host Immune Response in COVID-19

Jarai

Stillman

Bomb

et al. 2020

ACS Biomater. Sci. Eng.

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The COVID-19 pandemic caused by the global spread of the SARS-CoV-2 virus has led to a staggering number of deaths worldwide and significantly increased burden on healthcare as nations scramble to find mitigation strategies. While significant progress has been made in COVID-19 diagnostics and therapeutics, effective prevention and treatment options remain scarce. Because of the potential for the SARS-CoV-2 infections to cause systemic inflammation and multiple organ failure, it is imperative for the scientific community to evaluate therapeutic options aimed at modulating the causative host immune responses to prevent subsequent systemic complications. Harnessing decades of expertise in the use of natural and synthetic materials for biomedical applications, the biomaterials community has the potential to play an especially instrumental role in developing new strategies or repurposing existing tools to prevent or treat complications resulting from the COVID-19 pathology. Leveraging microparticle- and nanoparticle-based technology, especially in pulmonary delivery, biomaterials have demonstrated the ability to effectively modulate inflammation and may be well-suited for resolving SARS-CoV-2-induced effects. Here, we provide an overview of the SARS-CoV-2 virus infection and highlight current understanding of the host’s pulmonary immune response and its contributions to disease severity and systemic inflammation. Comparing to frontline COVID-19 therapeutic options, we highlight the most significant untapped opportunities in immune engineering of the host response using biomaterials and particle technology, which have the potential to improve outcomes for COVID-19 patients, and identify areas needed for future investigations. We hope that this work will prompt preclinical and clinical investigations of promising biomaterials-based treatments to introduce new options for COVID-19 patients.

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Modulating inflammatory macrophages with an apoptotic body-inspired nanoparticle

Cited by 48 publications

References 58 publications

Acute cardiometabolic effects of brief active breaks in sitting for patients with rheumatoid arthritis

Acute cardiometabolic effects of brief active breaks in sitting for patients with rheumatoid arthritis

Neutrophils and Macrophages as Targets for Development of Nanotherapeutics in Inflammatory Diseases

Biomaterials-Based Opportunities to Engineer the Pulmonary Host Immune Response in COVID-19

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