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Journal ArticleDOI

Anti-obesity and anti-inflammatory effects of macrophage-targeted interleukin-10-conjugated liposomes in obese mice.

TL;DR: The findings suggest that the PSL-IL10 has macrophage targeting ability and enhanced anti- inflammatory effect due to the synergistic anti-inflammatory effects of IL-10 and PSL, and can be used as amacrophage-targeted therapeutic material for inflammation-related diseases, including obesity.
About: This article is published in Biomaterials.The article was published on 2016-12-01. It has received 55 citations till now. The article focuses on the topics: Proinflammatory cytokine & Interleukin 10.
Citations
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Journal ArticleDOI
TL;DR: In this large, community-based sample, increased body-mass index was associated with an increased risk of heart failure and strategies to promote optimal body weight may reduce the population burden ofheart failure.

1,388 citations

Journal ArticleDOI
TL;DR: The review will discuss, at a pre-clinical stage, the main innovative nanomedicine approaches that have been proposed in the past five years for the resolution of inflammatory disorders, finally focusing on those currently in clinical trials.

79 citations


Cites background from "Anti-obesity and anti-inflammatory ..."

  • ...It was suggested that this association could be used as a macrophage-targeted therapy for inflammation-related diseases[69]....

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Journal ArticleDOI
TL;DR: The SeNPs may have potential as a theranostic nanomaterial to image and control the activation of macrophages and quenched the intracellular H2O2 and NO that are associated with inflammation.
Abstract: Macrophages have a pivotal role in chronic inflammatory diseases (CIDs), so imaging and controlling activated macrophage is critical for detecting and reducing chronic inflammation. In this study, photodynamic selenium nanoparticles (SeNPs) with photosensitive and macrophage-targeting bilayers were developed. The first layer of the photosensitive macromolecule was composed of a conjugate of a photosensitizer (rose bengal, RB) and a thiolated chitosan (chitosan-glutathione), resulting in a plasmonic coupling-induced red shift and broadening of RB absorption bands with increased absorption intensity. Electron paramagnetic resonance (EPR) and diphenylanthracene (DPA) quenching studies revealed that the SeNPs that were coated with the photosensitive layer were more effective than RB alone in producing singlet oxygen (1O2) under photoirradiation. The second layer of the activated macrophage-targetable macromolecule was synthesized by conjugation of hyaluronic acid with folic acid using an ethylenediamine linke...

66 citations

Journal ArticleDOI
22 Apr 2021
TL;DR: In this paper, Nanotrap surfaces were functionalized with either recombinant ACE2 proteins or anti-SARS-CoV-2 neutralizing antibodies and phagocytosis-specific phosphatidylserines.
Abstract: SARS-CoV-2 enters host cells through its viral spike protein binding to angiotensin-converting enzyme 2 (ACE2) receptors on the host cells. Here, we show that functionalized nanoparticles, termed "Nanotraps," completely inhibited SARS-CoV-2 infection by blocking the interaction between the spike protein of SARS-CoV-2 and the ACE2 of host cells. The liposomal-based Nanotrap surfaces were functionalized with either recombinant ACE2 proteins or anti-SARS-CoV-2 neutralizing antibodies and phagocytosis-specific phosphatidylserines. The Nanotraps effectively captured SARS-CoV-2 and completely blocked SARS-CoV-2 infection to ACE2-expressing human cell lines and primary lung cells; the phosphatidylserine triggered subsequent phagocytosis of the virus-bound, biodegradable Nanotraps by macrophages, leading to the clearance of pseudotyped and authentic virus in vitro. Furthermore, the Nanotraps demonstrated an excellent biosafety profile in vitro and in vivo. Finally, the Nanotraps inhibited pseudotyped SARS-CoV-2 infection in live human lungs in an ex vivo lung perfusion system. In summary, Nanotraps represent a new nanomedicine for the inhibition of SARS-CoV-2 infection.

31 citations

Journal ArticleDOI
TL;DR: The influence of faba bean seed fermentation on the release of bioactive peptides after digestion in gastrointestinal conditions was investigated in this article, where the molecular mass of protein detected by SDS-PAGE was in the range from 6.5 to 97.kDa.
Abstract: The influence of faba bean seed fermentation on the release of bioactive peptides after digestion in gastrointestinal conditions was investigated. The molecular mass of protein detected by SDS-PAGE was in the range from 6.5 to 97 kDa. The highest degree of protein hydrolysis (98.72%) was noted for protein obtained from seeds fermented for 3 h at 37 °C. The hydrolyzate of seeds fermented for 7 days at 30 °C was characterized by the highest peptide content (4.78 mg/mL). The highest ACE-inhibitory and antiradical against ABTS·+ activity were noted for a peptide fraction obtained from a sample fermented for 3 days at 30 °C (IC50 = 1.01 and 0.99 mg/mL, respectively). The sample obtained after 3-h fermentation at 22 °C was characterized by the highest LOX inhibitory activity (IC50 = 0.54 mg/mL). The lowest IC50 value was determined for fractions obtained from seeds fermented for 3 h and 7 days at 37 °C, and the value was not significantly different (0.92 and 0.89 mg/mL, respectively). The peptide fraction obtained from seeds fermented for 3 days at 30 °C with the highest potential for inhibition of metabolic syndrome development was separated on Sephadex G10 and peptide sequences were identified by LC-MS/MS.

31 citations

References
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Journal ArticleDOI
TL;DR: Transcript expression in perigonadal adipose tissue from groups of mice in which adiposity varied due to sex, diet, and the obesity-related mutations agouti (Ay) and obese (Lepob) found that the expression of 1,304 transcripts correlated significantly with body mass.
Abstract: Obesity alters adipose tissue metabolic and endocrine function and leads to an increased release of fatty acids, hormones, and proinflammatory molecules that contribute to obesity associated complications. To further characterize the changes that occur in adipose tissue with increasing adiposity, we profiled transcript expression in perigonadal adipose tissue from groups of mice in which adiposity varied due to sex, diet, and the obesity-related mutations agouti (Ay) and obese (Lepob). We found that the expression of 1,304 transcripts correlated significantly with body mass. Of the 100 most significantly correlated genes, 30% encoded proteins that are characteristic of macrophages and are positively correlated with body mass. Immunohistochemical analysis of perigonadal, perirenal, mesenteric, and subcutaneous adipose tissue revealed that the percentage of cells expressing the macrophage marker F4/80 (F4/80+) was significantly and positively correlated with both adipocyte size and body mass. Similar relationships were found in human subcutaneous adipose tissue stained for the macrophage antigen CD68. Bone marrow transplant studies and quantitation of macrophage number in adipose tissue from macrophage-deficient (Csf1op/op) mice suggest that these F4/80+ cells are CSF-1 dependent, bone marrow-derived adipose tissue macrophages. Expression analysis of macrophage and nonmacrophage cell populations isolated from adipose tissue demonstrates that adipose tissue macrophages are responsible for almost all adipose tissue TNF-alpha expression and significant amounts of iNOS and IL-6 expression. Adipose tissue macrophage numbers increase in obesity and participate in inflammatory pathways that are activated in adipose tissues of obese individuals.

8,902 citations

Journal ArticleDOI
14 Dec 2006-Nature
TL;DR: In obese individuals, adipose tissue releases increased amounts of non-esterified fatty acids, glycerol, hormones, pro-inflammatory cytokines and other factors that are involved in the development of insulin resistance.
Abstract: Obesity is associated with an increased risk of developing insulin resistance and type 2 diabetes In obese individuals, adipose tissue releases increased amounts of non-esterified fatty acids, glycerol, hormones, pro-inflammatory cytokines and other factors that are involved in the development of insulin resistance When insulin resistance is accompanied by dysfunction of pancreatic islet beta-cells - the cells that release insulin - failure to control blood glucose levels results Abnormalities in beta-cell function are therefore critical in defining the risk and development of type 2 diabetes This knowledge is fostering exploration of the molecular and genetic basis of the disease and new approaches to its treatment and prevention

4,515 citations


"Anti-obesity and anti-inflammatory ..." refers background in this paper

  • ...Obesity is a risk factor for several diseases, including chronic kidney disease [1], non-alcoholic fatty liver disease [2], type 2 diabetes [3,4], and cardiovascular diseases [5,6]....

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Journal ArticleDOI
TL;DR: Diet-induced obesity leads to a shift in the activation state of ATMs from an M2-polarized state in lean animals that may protect adipocytes from inflammation to an M1 proinflammatory state that contributes to insulin resistance.
Abstract: Adipose tissue macrophages (ATMs) infiltrate adipose tissue during obesity and contribute to insulin resistance. We hypothesized that macrophages migrating to adipose tissue upon high-fat feeding may differ from those that reside there under normal diet conditions. To this end, we found a novel F4/80(+)CD11c(+) population of ATMs in adipose tissue of obese mice that was not seen in lean mice. ATMs from lean mice expressed many genes characteristic of M2 or "alternatively activated" macrophages, including Ym1, arginase 1, and Il10. Diet-induced obesity decreased expression of these genes in ATMs while increasing expression of genes such as those encoding TNF-alpha and iNOS that are characteristic of M1 or "classically activated" macrophages. Interestingly, ATMs from obese C-C motif chemokine receptor 2-KO (Ccr2-KO) mice express M2 markers at levels similar to those from lean mice. The antiinflammatory cytokine IL-10, which was overexpressed in ATMs from lean mice, protected adipocytes from TNF-alpha-induced insulin resistance. Thus, diet-induced obesity leads to a shift in the activation state of ATMs from an M2-polarized state in lean animals that may protect adipocytes from inflammation to an M1 proinflammatory state that contributes to insulin resistance.

4,046 citations


"Anti-obesity and anti-inflammatory ..." refers background in this paper

  • ...In contrast, an increase in antiinflammatory M2 macrophages in ATs upregulates the expression of anti-inflammatory cytokine IL-10 and protects adipocytes from TNF-a-induced insulin resistance [10,12]....

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  • ...These ATMs are a major source of proinflammatory molecules in the adipocyte-mediated inflammatory response [9,10]....

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  • ...) secreted by ATMs and elevated in obesity [9,10]....

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Journal ArticleDOI
TL;DR: There was an increase in the risk of heart failure of 5 percent for men and 7 percent for women for each increment of 1 in body-mass index after adjustment for established risk factors.
Abstract: Background Extreme obesity is recognized to be a risk factor for heart failure. It is unclear whether overweight and lesser degrees of obesity also pose a risk. Methods We investigated the relation between the body-mass index (the weight in kilograms divided by the square of the height in meters) and the incidence of heart failure among 5881 participants in the Framingham Heart Study (mean age, 55 years; 54 percent women). With the use of Cox proportional-hazards models, the body-mass index was evaluated both as a continuous variable and as a categorical variable (normal, 18.5 to 24.9; overweight, 25.0 to 29.9; and obese, 30.0 or more). Results During follow-up (mean, 14 years), heart failure developed in 496 subjects (258 women and 238 men). After adjustment for established risk factors, there was an increase in the risk of heart failure of 5 percent for men and 7 percent for women for each increment of 1 in body-mass index. As compared with subjects with a normal body-mass index, obese subjects had a do...

2,499 citations

Journal ArticleDOI
TL;DR: It is demonstrated that >90% of all macrophages in WAT of obese mice and humans are localized to dead adipocytes, where they fuse to form syncytia that sequester and scavenge the residual “free” adipocyte lipid droplet and ultimately form multinucleate giant cells, a hallmark of chronic inflammation.

2,235 citations