Different capacities of Staphyloccocus aureus and Staphyloccocus epidermidis isolated from patients, to activate innate immune cells

2.47 SILVIA DÁVILA, SARA SATORRES, JULIO ARCE MIRANDA, MARIA GABRIELA PARAJE, CLAUDIA M. MATTANA, VIRGINIA RIVERO.

Congreso; VI Congreso Argentino de Microbiología General; 2009

Most of species of the genus Staphyloccocus are widely distributed in the nature, and are essential commensal of the normal bacterial flora in human skin and mucosa. Nevertheless, Staphyloccocus epidermidis is important as the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, skin and mucosa. Nevertheless, Staphyloccocus epidermidis is important as the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, nature, and are essential commensal of the normal bacterial flora in human skin and mucosa. Nevertheless, Staphyloccocus epidermidis is important as the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, skin and mucosa. Nevertheless, Staphyloccocus epidermidis is important as the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, Staphyloccocus are widely distributed in the nature, and are essential commensal of the normal bacterial flora in human skin and mucosa. Nevertheless, Staphyloccocus epidermidis is important as the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, skin and mucosa. Nevertheless, Staphyloccocus epidermidis is important as the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, and are essential commensal of the normal bacterial flora in human skin and mucosa. Nevertheless, Staphyloccocus epidermidis is important as the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, and mucosa. Nevertheless, Staphyloccocus epidermidis is important as the main pathogen in foreign body infections, where it does not induce a significant systemic or local inflammatory response. On the other hand, Staphyloccocus aureus is a well characterized specie, known to have a diverse arsenal of virulence factors and to cause skin superficial or invasive serious infections accompanied with a prominent inflammatory response. diverse arsenal of virulence factors and to cause skin superficial or invasive serious infections accompanied with a prominent inflammatory response. is a well characterized specie, known to have a diverse arsenal of virulence factors and to cause skin superficial or invasive serious infections accompanied with a prominent inflammatory response. In the present work, we studied the capacity of different clinical strains of S. epidermidis and S. aureus to stimulate macrophages or epithelial cells. We analyzed the production nitric oxide (NO) or urea, two intermediaries from the arginine metabolism that involve nitric oxide synthase enzyme (which generates NO, an inflammatory mediator) and arginase enzyme (which generates urea, depleting the milieu of arginine with an anti-inflammatory outcome). Sixteen clinical strains of S. aureus and 11 clinical strains of S. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. analyzed the production nitric oxide (NO) or urea, two intermediaries from the arginine metabolism that involve nitric oxide synthase enzyme (which generates NO, an inflammatory mediator) and arginase enzyme (which generates urea, depleting the milieu of arginine with an anti-inflammatory outcome). Sixteen clinical strains of S. aureus and 11 clinical strains of S. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. epidermidis and S. aureus to stimulate macrophages or epithelial cells. We analyzed the production nitric oxide (NO) or urea, two intermediaries from the arginine metabolism that involve nitric oxide synthase enzyme (which generates NO, an inflammatory mediator) and arginase enzyme (which generates urea, depleting the milieu of arginine with an anti-inflammatory outcome). Sixteen clinical strains of S. aureus and 11 clinical strains of S. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. analyzed the production nitric oxide (NO) or urea, two intermediaries from the arginine metabolism that involve nitric oxide synthase enzyme (which generates NO, an inflammatory mediator) and arginase enzyme (which generates urea, depleting the milieu of arginine with an anti-inflammatory outcome). Sixteen clinical strains of S. aureus and 11 clinical strains of S. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. S. epidermidis and S. aureus to stimulate macrophages or epithelial cells. We analyzed the production nitric oxide (NO) or urea, two intermediaries from the arginine metabolism that involve nitric oxide synthase enzyme (which generates NO, an inflammatory mediator) and arginase enzyme (which generates urea, depleting the milieu of arginine with an anti-inflammatory outcome). Sixteen clinical strains of S. aureus and 11 clinical strains of S. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. analyzed the production nitric oxide (NO) or urea, two intermediaries from the arginine metabolism that involve nitric oxide synthase enzyme (which generates NO, an inflammatory mediator) and arginase enzyme (which generates urea, depleting the milieu of arginine with an anti-inflammatory outcome). Sixteen clinical strains of S. aureus and 11 clinical strains of S. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. and S. aureus to stimulate macrophages or epithelial cells. We analyzed the production nitric oxide (NO) or urea, two intermediaries from the arginine metabolism that involve nitric oxide synthase enzyme (which generates NO, an inflammatory mediator) and arginase enzyme (which generates urea, depleting the milieu of arginine with an anti-inflammatory outcome). Sixteen clinical strains of S. aureus and 11 clinical strains of S. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. S. aureus and 11 clinical strains of S. epidermidis isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. isolated from blood cultures and catheters of hospitalized patients, were included in our study. Bacteria were incubated with RAW 264.7 or A549 cells and 48 hours later NO production and arginase activity were evaluated by the Griess’s technique or measuring urea levels respectively. Our results showed significant differences in the capacities of S. epidermidisS. epidermidis or S. aureus to stimulate macrophages and epithelial cells. Strains of S. aureus included in our study showed higher capacity to induce NO in RAW 264.7 (p<0.05) and A549 cells. When we analyzed the abilities of both species to induce arginase activity, we observed that S. aureus and S. epidermidis were poor inductors of arginase activity exhibiting no differences among species. Our results demonstrate that S. aureus was good inductor of NO while S. epidermidis exhibited scarce ability to induce this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. good inductor of NO while S. epidermidis exhibited scarce ability to induce this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. differences among species. Our results demonstrate that S. aureus was good inductor of NO while S. epidermidis exhibited scarce ability to induce this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. good inductor of NO while S. epidermidis exhibited scarce ability to induce this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. epidermidis were poor inductors of arginase activity exhibiting no differences among species. Our results demonstrate that S. aureus was good inductor of NO while S. epidermidis exhibited scarce ability to induce this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. good inductor of NO while S. epidermidis exhibited scarce ability to induce this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. differences among species. Our results demonstrate that S. aureus was good inductor of NO while S. epidermidis exhibited scarce ability to induce this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. not related to a deviation bias the arginase metabolic way. In conclusion, our results show that S. aureus and S. epidermidis present different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. different capacity to stimulate cells of innate immunity, and suggest that this characteristic might explain the different clinical presentation observed in patients affected by these microorganisms. this inflammatory mediator in macrophage and epithelial cells. Our results also demonstrated that the low capacity of S. epidermidis to induce NO, was not related to a deviation bias the arginase metabolic way. In conclusion, our