Effect of Functional Stimulation on Ascorbate Content in Phagocytes under Physiological and Pathological Conditions

Oberritter, H; Glatthaar, Beat E.; Moser, Ulrich; Schmidt, Karl‐Heinz

doi:10.1159/000234106

Cited by 43 publications

(35 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Macrophages normally accumulate and maintain very high intracellular levels of AA compared with plasma via specific sodium-dependent transporters, thus providing an effective mechanism to neutralize excessive ROS in these cells (40). However, levels of intracellular AA can be significantly decreased after activation of phagocytosis (52). Thus, AA supplementation under oxidative stress may help to maintain the levels of intracellular AA, and subsequently the antioxidant capacity of the alveolar macrophages during phagocytosis, leading to the improvement in phagocytic activity, as in the results shown in Figure 2.…”

Section: Discussionmentioning

confidence: 99%

Ascorbic Acid Attenuates Hyperoxia-Compromised Host Defense against Pulmonary Bacterial Infection

Patel

Sampat

Espey

et al. 2016

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Supraphysiological concentrations of oxygen (hyperoxia) can compromise host defense and increase susceptibility to bacterial infections, causing ventilator-associated pneumonia. The phagocytic activity of macrophages is impaired by hyperoxia-induced increases in the levels of reactive oxygen species (ROS) and extracellular highmobility group box protein B1 (HMGB1). Ascorbic acid (AA), an essential nutrient and antioxidant, has been shown to be beneficial in various animal models of ROS-mediated diseases. The aim of this study was to determine whether AA could attenuate hyperoxiacompromised host defense and improve macrophage functions against bacterial infections. C57BL/6 male mice were exposed to hyperoxia (>98% O 2 , 48 h), followed by intratracheal inoculation with Pseudomonas aeruginosa, and simultaneous intraperitoneal administration of AA. AA (50 mg/kg) significantly improved bacterial clearance in the lungs and airways, and significantly reduced HMGB1 accumulation in the airways. The incubation of RAW 264.7 cells (a macrophage-like cell line) with AA (0-1,000 mM) before hyperoxic exposure (95% O 2 ) stabilized the phagocytic activity of macrophages in a concentration-dependent manner. The AA-enhanced macrophage function was associated with significantly decreased production of intracellular ROS and accumulation of extracellular HMGB1. These data suggest that AA supplementation can prevent or attenuate the development of ventilator-associated pneumonia in patients receiving oxygen support.

show abstract

Section: Discussionmentioning

confidence: 99%

Ascorbic Acid Attenuates Hyperoxia-Compromised Host Defense against Pulmonary Bacterial Infection

Patel

Sampat

Espey

et al. 2016

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

show abstract

“…Here, ascorbic acid could prevent the oxi dative inactivation of a ¡-proteinase inhibitor (a ¡-PI) (17). Upon phagocytosis, the ascorbic acid content of neutrophils decreases (18).…”

Section: Introductionmentioning

confidence: 99%

“…Vitamin C concentrations in plasma are low in critically ill patients admitted to the intensive care unit (19), in patients with rheumatoid arthritis (18,20) and bronchial asthma (21), and in smokers (22); each is a condition that involves the activation of white blood cells (WBCs) and ROS generation.…”

Section: Introductionmentioning

confidence: 99%

Plasma vitamin C concentrations in patients with cystic fibrosis: evidence of associations with lung inflammation

Winklhofer‐Roob

Ellemunter

Frühwirth

et al. 1997

The American Journal of Clinical Nutrition

View full text Add to dashboard Cite

Vitamin C status and possible associations with the disease process in cystic fibrosis (CP) patients were investi gated. Plasma vitamin C concentrations in patients from two different mid-European populations (Swiss, n = 62; Austrian, /j -60) taking no or low-dose vitamin C from multivitamin supplements did not differ from each oilier or from control subjects (» ~ 34). Vitamin C concentrations decreased with age (5,05 /xmol ■ L 1 • y~ '). When followed up for 12 mo, patients had the highest plasma vitamin C concentrations in February and the lowest in May and August (P < 0.01); the decrease in vitamin C was accompanied by increases in plasma malondialdehyde (P < 0.001) and tumor necrosis factor a concentrations (P < 0.01). During supplementation with vitamin E for 2 mo or /3-carotene for 12 mo vitamin C concentrations did not change. They correlated inversely with white blood cell count (r --0.36, P = 0.008), bands (r --0.36, P = 0.02), a j-acid glycoprotein (/* --0.45, P = 0.002), interleukin 6 (r = -0.46, P = 0.0006), and neutrophil elastase/a,-proteinase inhibitor complexes (r = -0.34, P ~ 0.02). In patients with vitamin C concentrations < 40 /xmol/L, all in dexes of inflammation were relatively high, whereas those with concentrations > 80 /¿mol/L (upper quartile of control subjects) showed clearly lower values. These results are consistent with the hypothesis that by scavenging oxygen free radicals vitamin C interacts with an in lì am mat ion-amplifying cycle of activation of alveolar macrophages and neutrophils, release of proinflammatory cytokines and oxygen free radicals, and inactivation of anti pro teases, Am J Clin Nutr 1997;65:1858-66.

show abstract

“…Circumstantial evidence suggests that ascorbate is important. For example, the ascorbate content of macrophages is estimated to be several-fold higher than that of neutrophils and 40-60 times that of plasma (Oberritter et al, 1986). Further, phagocytosis of zymosan by macrophages decreased endogenous intracellular ascorbate concentrations, leading to the hypothesis that ascorbate is protective to the cells (Oberritter et al, 1986).…”

Section: Macrophagesmentioning

confidence: 99%

“…For example, the ascorbate content of macrophages is estimated to be several-fold higher than that of neutrophils and 40-60 times that of plasma (Oberritter et al, 1986). Further, phagocytosis of zymosan by macrophages decreased endogenous intracellular ascorbate concentrations, leading to the hypothesis that ascorbate is protective to the cells (Oberritter et al, 1986). In recent studies of thioglycollate-elicited mouse peritoneal macrophages (May et al, 2005b), ascorbate loading to intracellular concentrations of 3-10 mM prevented oxidant stress induced by latex beads.…”

Section: Macrophagesmentioning

confidence: 99%

Inflammation in the vascular bed: Importance of vitamin C

Aguirre

May

2008

Pharmacology & Therapeutics

110

View full text Add to dashboard Cite

Despite decreases in atherosclerotic coronary vascular disease over the last several decades, atherosclerosis remains a major cause of mortality in developed nations. One possible contributor to this residual risk is oxidant stress, which is generated by the inflammatory response of atherosclerosis. Although there is a wealth of in vitro, cellular, and animal data supporting a protective role for antioxidant vitamins and nutrients in the atherosclerotic process, the best clinical trials have been negative. This may be due to the fact that antioxidant therapies are applied "too little and too late." This review considers the role of vitamin C, or ascorbic acid in preventing the earliest inflammatory changes in atherosclerosis. It focuses on the three major vascular cell types involved in atherosclerosis: endothelial cells, vascular smooth muscle cells, and macrophages. Ascorbate chemistry, recycling, and function are described for these cell types, with emphasis on whether and how the vitamin might affect the inflammatory process. For endothelial cells, ascorbate helps to prevent endothelial dysfunction, stimulates type IV collagen synthesis, and enhances cell proliferation. For vascular smooth muscle cells, ascorbate inhibits dedifferentiation, recruitment, and proliferation in areas of vascular damage. For macrophages, ascorbate decreases oxidant stress related to their activation, decreases uptake and degradation of oxidized LDL in some studies, and enhances several aspects of their function. Although further studies of ascorbate function in these cell types and in novel animal models are needed, available evidence generally supports a salutary role for this vitamin in ameliorating the earliest stages of atherosclerosis.

show abstract

Effect of Functional Stimulation on Ascorbate Content in Phagocytes under Physiological and Pathological Conditions

Cited by 43 publications

References 26 publications

Ascorbic Acid Attenuates Hyperoxia-Compromised Host Defense against Pulmonary Bacterial Infection

Ascorbic Acid Attenuates Hyperoxia-Compromised Host Defense against Pulmonary Bacterial Infection

Plasma vitamin C concentrations in patients with cystic fibrosis: evidence of associations with lung inflammation

Inflammation in the vascular bed: Importance of vitamin C

Contact Info

Product

Resources

About