arginase/inflammatie

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Helminth-induced arginase-1 exacerbates lung inflammation and disease severity in tuberculosis.

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Parasitic helminth worms, such as Schistosoma mansoni, are endemic in regions with a high prevalence of tuberculosis (TB) among the population. Human studies suggest that helminth coinfections contribute to increased TB susceptibility and increased rates of TB reactivation. Prevailing models suggest

Extracellular activation of arginase-1 decreases enterocyte inducible nitric oxide synthase activity during systemic inflammation.

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Liver dysfunction secondary to severe inflammation is associated with the release of enzymes normally sequestered within hepatocytes. The purpose of these studies was to test the hypothesis that these enzymes are released, at least in part, to modulate potentially deleterious inflammatory processes

The arginine-arginase balance in asthma and lung inflammation.

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Asthma, a complex chronic inflammatory pulmonary disorder, is on the rise despite intense ongoing research underscoring the need for new scientific inquiry. Using global microarray analysis, we have recently uncovered that asthmatic responses involve metabolism of arginine by arginase. We found that

Cell- and isoform-specific increases in arginase expression in acute silica-induced pulmonary inflammation.

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Arginase induction was reported in several inflammatory lung diseases, suggesting that this may be a common feature underlying the pathophysiology of such diseases. As little is known regarding arginase expression in silicosis, the induction and cellular localization of arginase were elucidated in

Anti-inflammatory effect of arginase inhibitor and corticosteroid on airway allergic reactions in a Dermatophogoides farinae-induced NC/Nga mouse model.

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The present study was aimed to investigate the effect of an arginase inhibitor, N-hydroxy-nor-L-arginine (nor-NOHA) and a corticosteroid, prednisolone, in an intranasal mite-induced NC/Nga mouse model of asthma. The treatment with nor-NOHA and prednisolone inhibited the increase in airway

The arginase II gene is an anti-inflammatory target of liver X receptor in macrophages.

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The liver X receptors (LXRs) are ligand-dependent transcription factors that have been implicated in lipid metabolism and inflammation. LXRs also inhibit the expression of inflammatory genes in macrophages, including inducible nitric oxide synthase (iNOS). Some of these actions are mediated through

Arginase inhibition ameliorates adipose tissue inflammation in mice with diet-induced obesity.

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This study examined whether oral administration of an arginase inhibitor regulates adipose tissue macrophage infiltration and inflammation in mice with high fat diet (HFD)-induced obesity. Male C57BL/6 mice (n = 30) were randomly assigned to control (CTL, n = 10), HFD only (n = 10), and HFD with

Personal Ozone Exposure and Respiratory Inflammatory Response: The Role of DNA Methylation in the Arginase-Nitric Oxide Synthase Pathway.

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Little is known regarding the molecular mechanisms behind respiratory inflammatory response induced by ozone. We performed a longitudinal panel study with four repeated measurements among 43 young adults in Shanghai, China from May to October in 2016. We collected buccal samples and measured the

The potential inflammatory role of arginase and iNOS in children with chronic adenotonsillar hypertrophy.

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OBJECTIVE Nitric oxide (NO) induced tissue damage has been implicated in the pathogenesis of several diseases. Although recurrent/chronic tonsillitis and hypertrophy are still the most frequent surgical procedures carried out on children in order to cure these pathologies, etiopathogenetic

Effect of Pneumoperitoneum on Oxidative Stress and Inflammation via the Arginase Pathway in Rats.

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OBJECTIVE Oxidative stress during CO₂ pneumoperitoneum is reported to be associated with decreased bioactivity of nitric oxide (NO). However, the changes in endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and arginase during CO₂ pneumoperitoneum have not been

Arginase I suppresses IL-12/IL-23p40-driven intestinal inflammation during acute schistosomiasis.

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Alternatively activated macrophages prevent lethal intestinal pathology caused by worm ova in mice infected with the human parasite Schistosoma mansoni through mechanisms that are currently unclear. This study demonstrates that arginase I (Arg I), a major product of IL-4- and IL-13-induced

Arginase I attenuates inflammatory cytokine secretion induced by lipopolysaccharide in vascular smooth muscle cells.

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OBJECTIVE Inflammation plays an important role in atherosclerosis. Arginase I (Arg I) promotes the proliferation of vascular smooth muscle cells; however, the effect of Arg I on inflammation remains unknown. The present study investigated the role of Arg I in inflammation in vitro and in

Arginase activity mediates retinal inflammation in endotoxin-induced uveitis.

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Arginase has been reported to reduce nitric oxide bioavailability in cardiovascular disease. However, its specific role in retinopathy has not been studied. In this study, we assessed the role of arginase in a mouse model of endotoxin-induced uveitis induced by lipopolysaccharide (LPS) treatment.

Human papillomavirus e7 oncoprotein transgenic skin develops an enhanced inflammatory response to 2,4-dinitrochlorobenzene by an arginase-1-dependent mechanism.

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We have shown that the expression of human papillomavirus type 16 E7 (HPV16.E7) protein within epithelial cells results in local immune suppression and a weak and ineffective immune response to E7 similar to that occuring in HPV-associated premalignancy and cancers. However, a robust acute

Serum fetuin-A and arginase-1 in human obesity model: Is there any interaction between inflammatory status and arginine metabolism?

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Obesity is a major risk factor for many chronic metabolic diseases such as inflammation, insulin resistance (IR) and fatty liver injury. It was reported that obesity causes some variations on the serum levels of fetuin-A and is associated with arginine metabolism, especially arginase-1 levels. The

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