The crucial role of l-arginine in macrophage activation: What you need to know about it

Pekarová, Michaela; Lojek, Antonı́n

doi:10.1016/j.lfs.2015.07.012

Cited by 29 publications

(22 citation statements)

References 81 publications

(48 reference statements)

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“…The amino acid l -arginine is classified as “conditionally essential,” depending on the developmental state and health status of an individual (6). During an infection, l -arginine availability has been shown to be a crucial regulator of immune functions, and several pathogens, such as Salmonella and Leishmania spp., can impact host l -arginine metabolism in various ways (4).…”

Section: Discussionmentioning

confidence: 99%

“…The availability of l -arginine is a rate-limiting factor in NO synthesis (6), and in mammalian cells, iNOS competes with the enzyme arginase-1 (Arg-1) for the substrate l -arginine. Arginase-1 can be induced in macrophages by type 2 cytokines, such as IL-4, IL-13, IL-10, and transforming growth factor beta (TGF-β), inhibiting iNOS functions and leading to increased humoral immunity, tissue repair, and allergic responses (7).…”

Section: Introductionmentioning

confidence: 99%

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Candida albicans Chitin Increases Arginase-1 Activity in Human Macrophages, with an Impact on Macrophage Antimicrobial Functions

Wagener

MacCallum

Brown

et al. 2017

mBio

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The opportunistic human fungal pathogen Candida albicans can cause a variety of diseases, ranging from superficial mucosal infections to life-threatening systemic infections. Phagocytic cells of the innate immune response, such as neutrophils and macrophages, are important first-line responders to an infection and generate reactive oxygen and nitrogen species as part of their protective antimicrobial response. During an infection, host cells generate nitric oxide through the enzyme inducible nitric oxide synthase (iNOS) to kill the invading pathogen. Inside the phagocyte, iNOS competes with the enzyme arginase-1 for a common substrate, the amino acid l-arginine. Several pathogenic species, including bacteria and parasitic protozoans, actively modulate the production of nitric oxide by inducing their own arginases or the host’s arginase activity to prevent the conversion of l-arginine to nitric oxide. We report here that C. albicans blocks nitric oxide production in human-monocyte-derived macrophages by induction of host arginase activity. We further determined that purified chitin (a fungal cell wall polysaccharide) and increased chitin exposure at the fungal cell wall surface induces this host arginase activity. Blocking the C. albicans-induced arginase activity with the arginase-specific substrate inhibitor Nω-hydroxy-nor-arginine (nor-NOHA) or the chitinase inhibitor bisdionin F restored nitric oxide production and increased the efficiency of fungal killing. Moreover, we determined that C. albicans influences macrophage polarization from a classically activated phenotype toward an alternatively activated phenotype, thereby reducing antimicrobial functions and mediating fungal survival. Therefore, C. albicans modulates l-arginine metabolism in macrophages during an infection, potentiating its own survival.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Candida albicans Chitin Increases Arginase-1 Activity in Human Macrophages, with an Impact on Macrophage Antimicrobial Functions

Wagener

MacCallum

Brown

et al. 2017

mBio

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“…Omega-3 fatty acids down regulate the TNF-a response to lip polysaccharide insult, as would be seen in sepsis and this may have a direct role in Hepatoprotection (Udristioiu et al, 2014). Pekarova and Lojek (2015) demonstrated that Larginine serves as a precursor in protein synthesis, and it is a substrate for a number of enzymes, including nitric oxide synthase (NOS), arginase, arginine glycine aminotransferase, and arginine decarboxylase, yielding nitric oxide (NO) and citrulline, ornithine and urea, creatine, and agmatine, respectively. These findings were in line with other study done by Lai et al (2015) supposing that oxidative stress play a crucial role in the pathogenesis of VPA induced hepatotoxicity.…”

Section: Discussionmentioning

confidence: 99%

The amelorative effect of L-arginin and omega-3 fatty acid against sodium valproate induced hepatotoxicity

Dalia¹,

Marwa²,

Walaa³

et al. 2018

J. Toxicol. Environ. Health Sci.

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Sodium valproate (VPA) used in epilepsy and has hepatotoxic effect in mammals. This work is to assess the role of L-arginin and omega-3 fatty acid against VPA oxidative stress on liver. This study was carried out on 70 rats divided into 7 groups each of 10 rats treated orally once daily 6days/ week; Group I (control), Group II (L-arginin): each rat was received 300 mg/kg L-arginin, Group III (omega-3): each rat received 300 mg/kg omega-3, Group IV (VIA): Each rat received 400 mg/kg VPA. Group V (VPA and L-arginin): Each rat received the previous doses. Group VI (VPA and omega-3): as before. Group VII (VPA, L-arginin and omega-3 group): as before. There was a significant increase in the mean values of AST, ALT, ALP and TBL in VPA treated group. Upon supplementation with L-arginin or omega-3 to VPA treated rats there was a significant decrease in the mean values of AST, ALT, ALP and TBL. Microscopic examination of liver section of VPA treated rat revealed vacuolated hepatocytes, focal necrosis, and enlarged portal tract. VPA toxicity induced severe liver damage in rats, and administration of either L-arginin or omega-3 protecting liver tissues.

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“…Recent studies suggested that amino acids act as signaling molecules in the periphery (Wu, 2013; Pekarova and Lojek, 2015). Since L-NAME, an inhibitor for nitric oxide synthase, had no effects upon the enhancement of Venus expression by intraportal Arg in the insular cortex, it seems that nitric oxide is not participated in the enhancement of Venus expression in the insular cortex.…”

Section: Discussionmentioning

confidence: 99%

Common Hepatic Branch of Vagus Nerve-Dependent Expression of Immediate Early Genes in the Mouse Brain by Intraportal L-Arginine: Comparison with Cholecystokinin-8

et al. 2017

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Information from the peripheral organs is thought to be transmitted to the brain by humoral factors and neurons such as afferent vagal or spinal nerves. The common hepatic branch of the vagus (CHBV) is one of the main vagus nerve branches, and consists of heterogeneous neuronal fibers that innervate multiple peripheral organs such as the bile duct, portal vein, paraganglia, and gastroduodenal tract. Although, previous studies suggested that the CHBV has a pivotal role in transmitting information on the status of the liver to the brain, the details of its central projections remain unknown. The purpose of the present study was to investigate the brain regions activated by the CHBV. For this purpose, we injected L-arginine or anorexia-associated peptide cholecystokinin-8 (CCK), which are known to increase CHBV electrical activity, into the portal vein of transgenic Arc-dVenus mice expressing the fluorescent protein Venus under control of the activity-regulated cytoskeleton-associated protein (Arc) promotor. The brain slices were prepared from these mice and the number of Venus positive cells in the slices was counted. After that, c-Fos expression in these slices was analyzed by immunohistochemistry using the avidin-biotin-peroxidase complex method. Intraportal administration of L-arginine increased the number of Venus positive or c-Fos positive cells in the insular cortex. This action of L-arginine was not observed in CHBV-vagotomized Arc-dVenus mice. In contrast, intraportal administration of CCK did not increase the number of c-Fos positive or Venus positive cells in the insular cortex. Intraportal CCK induced c-Fos expression in the dorsomedial hypothalamus, while intraportal L-arginine did not. This action of CCK was abolished by CHBV vagotomy. Intraportal L-arginine reduced, while intraportal CCK increased, the number of c-Fos positive cells in the nucleus tractus solitarii in a CHBV-dependent manner. The present results suggest that the CHBV can activate different brain regions depending on the nature of the peripheral stimulus.

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The crucial role of l-arginine in macrophage activation: What you need to know about it

Cited by 29 publications

References 81 publications

Candida albicans Chitin Increases Arginase-1 Activity in Human Macrophages, with an Impact on Macrophage Antimicrobial Functions

Candida albicans Chitin Increases Arginase-1 Activity in Human Macrophages, with an Impact on Macrophage Antimicrobial Functions

The amelorative effect of L-arginin and omega-3 fatty acid against sodium valproate induced hepatotoxicity

Common Hepatic Branch of Vagus Nerve-Dependent Expression of Immediate Early Genes in the Mouse Brain by Intraportal L-Arginine: Comparison with Cholecystokinin-8

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