Metabolic syndrome agravates cardiovascular, oxidative and inflammatory dysfunction during the acute phase of Trypanosoma cruzi infection in mice

Lucchetti, Bruno Fernando Cruz; Boaretto, Natalia; Lopes, Fernanda Novi Cortegoso; Malvezi, Aparecida Donizette; Lovo‐Martins, Maria Isabel; Tatakihara, Vera Lúcia Hideko; Fattori, Victor; Pereira, Rito Santo; Verri, Waldiceu A.; Araújo, Eduardo José de Almeida; Pinge‐Filho, Phileno; Martins‐Pinge, Marli Cardoso

doi:10.1038/s41598-019-55363-9

Cited by 11 publications

(4 citation statements)

References 87 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We then examined if the anti-inflammatory effect of Au/TiO 2 and Au/ZrO 2 was related to antioxidant properties, as demonstrated in other conditions 10 , 11 . To investigate this issue, we measured the effect of Au/MOx NPs on intracellular reactive oxygen species (ROS) concentration.…”

Section: Resultsmentioning

confidence: 99%

Anti-inflammatory effect of gold nanoparticles supported on metal oxides

Fujita

Zysman

Elgrabli

et al. 2021

Sci Rep

View full text Add to dashboard Cite

Gold (Au) can be deposited as nanoparticles (NPs) smaller than 10 nm in diameter on a variety of metal oxide (MOx) NPs. Au/MOx have high catalytic performance and selective oxidation capacity which could have implications in terms of biological activity, and more specifically in modulation of the inflammatory reaction. Therefore, the aim of this study was to examine the effect of Au/TiO2, Au/ZrO2 and Au/CeO2 on viability, phagocytic capacity and inflammatory profile (TNF-α and IL-1β secretion) of murine macrophages. The most important result of this study is an anti-inflammatory effect of Au/MOx depending on the MOx nature with particle internalization and no alteration of cell viability and phagocytosis. The effect was dependent on the MOx NPs chemical nature (Au/TiO2 > Au/ZrO2 > Au/CeO2 if we consider the number of cytokines whose concentration was reduced by the NPs), and on the inflammatory mediator considered. The effect of Au/TiO2 NPs was not related to Au NPs size (at least in the case of Au/TiO2 NPs in the range of 3–8 nm). To the best of our knowledge, this is the first demonstration of an anti-inflammatory effect of Au/MOx.

show abstract

Section: Resultsmentioning

confidence: 99%

Anti-inflammatory effect of gold nanoparticles supported on metal oxides

Fujita

Zysman

Elgrabli

et al. 2021

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Although specific links exist between MAFLD and the parasitic infections discussed below, there is no general consensus for an important interrelationship. However, several lines of experimental evidence are present that infections caused by Plasmodium species, Schistosoma species, Toxoplasma gondii (T. gondii) and Trypanosoma cruzi (T. cruzi) are at the interface with MAFLD (Viriyavejakul et al 2014;Chen et al 2013;Huang et al 2018;Lucchetti et al 2019).…”

Section: Bacteria and Parasitesmentioning

confidence: 99%

“…cruzi is a protozoan that causes Chagas disease. T. cruzi infection in mice reduces hepatic steatosis and exacerbates TLR4-mediated hepatic inflammation (Onofrio et al 2015;Lucchetti et al 2019;Cabalén et al 2016) which could worsen steatohepatitis. From the opposite perspective, the metabolic syndrome also intensifies Chagas disease in mice during the acute phase of T. cruzi infection (Lucchetti et al 2019), suggesting an interrelationship between the metabolic syndrome, T. cruzi infection and MAFLD.…”

Section: Trypanosoma Cruzimentioning

confidence: 99%

Infections at the nexus of metabolic-associated fatty liver disease

et al. 2021

View full text Add to dashboard Cite

Metabolic-associated fatty liver disease (MAFLD) is a chronic liver disease that affects about a quarter of the world population. MAFLD encompasses different disease stadia ranging from isolated liver steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis and hepatocellular carcinoma. Although MAFLD is considered as the hepatic manifestation of the metabolic syndrome, multiple concomitant disease-potentiating factors can accelerate disease progression. Among these risk factors are diet, lifestyle, genetic traits, intake of steatogenic drugs, male gender and particular infections. Although infections often outweigh the development of fatty liver disease, pre-existing MAFLD could be triggered to progress towards more severe disease stadia. These combined disease cases might be underreported because of the high prevalence of both MAFLD and infectious diseases that can promote or exacerbate fatty liver disease development. In this review, we portray the molecular and cellular mechanisms by which the most relevant viral, bacterial and parasitic infections influence the progression of fatty liver disease and steatohepatitis. We focus in particular on how infectious diseases, including coronavirus disease-19, hepatitis C, acquired immunodeficiency syndrome, peptic ulcer and periodontitis, exacerbate MAFLD. We specifically underscore the synergistic effects of these infections with other MAFLD-promoting factors. Keywords Metabolic-associated fatty liver disease (MAFLD) • Non-alcoholic steatohepatitis (NASH) • Infectious diseases • Lipid metabolism • Liver • SARS-CoV-2 • Human immunodeficiency virus • Hepatitis C • Helicobacter pylori • Klebsiella pneumoniae

show abstract

“…Moreover, the parasite can exacerbate inflammation and aggravate obesity related metabolic disorders (e.g. atherosclerosis and NAFLD) during the acute phase of infection in obese mice, due to a high affinity for host cholesterol (33,34). Since the relationship between protozoa and adipose tissue has been reviewed (25,35), we herein did not have too much discussion about it.…”

Section: Introductionmentioning

confidence: 99%

Helminth and Host Crosstalk: New Insight Into Treatment of Obesity and Its Associated Metabolic Syndromes

Dai

Yang

et al. 2022

Front. Immunol.

View full text Add to dashboard Cite

Obesity and its associated Metabolic Syndromes (Mets) represent a global epidemic health problem. Metabolic inflammation, lipid accumulation and insulin resistance contribute to the progression of these diseases, thereby becoming targets for drug development. Epidemiological data have showed that the rate of helminth infection negatively correlates with the incidence of obesity and Mets. Correspondingly, numerous animal experiments and a few of clinic trials in human demonstrate that helminth infection or its derived molecules can mitigate obesity and Mets via induction of macrophage M2 polarization, inhibition of adipogenesis, promotion of fat browning, and improvement of glucose tolerance, insulin resistance and metabolic inflammation. Interestingly, sporadic studies also uncover that several helminth infections can reshape gut microbiota of hosts, which is intimately implicated in the pathogenesis of obesity and Mets. Overall, these findings indicate that the crosstalk between helminth and hosts may be a novel direction for obesity and Mets therapy. The present article reviews the molecular mechanism of how helminth masters immunity and metabolism in obesity.

show abstract

Metabolic syndrome agravates cardiovascular, oxidative and inflammatory dysfunction during the acute phase of Trypanosoma cruzi infection in mice

Cited by 11 publications

References 87 publications

Anti-inflammatory effect of gold nanoparticles supported on metal oxides

Anti-inflammatory effect of gold nanoparticles supported on metal oxides

Infections at the nexus of metabolic-associated fatty liver disease

Helminth and Host Crosstalk: New Insight Into Treatment of Obesity and Its Associated Metabolic Syndromes

Contact Info

Product

Resources

About