Assessment of Neutrophil Function in Patients with Septic Shock: Comparison of Methods

Wenisch, Christoph; Fladerer, Petra; Patruta, Sanda; Krause, Robert; Hörl, Walter H.

doi:10.1128/cdli.8.1.178-180.2001

Cited by 10 publications

(9 citation statements)

References 24 publications

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“…However, iron chelation has inhibitory effects on the replication of intra-macrophage Salmonella in iron starvation models based on another iron chelator, deferasirox 33 – 35 . We propose here that reduction of the available iron specifically in the SCV attenuates the production of hydroxyl radicals, which accounts for the capacity of these cells to limit intra-macrophage Salmonella growth 36 (Supplementary Fig. 14 ).…”

Section: Discussionmentioning

confidence: 91%

The hepcidin-ferroportin axis controls the iron content of Salmonella-containing vacuoles in macrophages

et al. 2018

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Macrophages release iron into the bloodstream via a membrane-bound iron export protein, ferroportin (FPN). The hepatic iron-regulatory hormone hepcidin controls FPN internalization and degradation in response to bacterial infection. Salmonella typhimurium can invade macrophages and proliferate in the Salmonella-containing vacuole (SCV). Hepcidin is reported to increase the mortality of Salmonella-infected animals by increasing the bacterial load in macrophages. Here we assess the iron levels and find that hepcidin increases iron content in the cytosol but decreases it in the SCV through FPN on the SCV membrane. Loss-of-FPN from the SCV via the action of hepcidin impairs the generation of bactericidal reactive oxygen species (ROS) as the iron content decreases. We conclude that FPN is required to provide sufficient iron to the SCV, where iron serves as a cofactor for the generation of antimicrobial ROS rather than as a nutrient for Salmonella.

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Section: Discussionmentioning

confidence: 91%

The hepcidin-ferroportin axis controls the iron content of Salmonella-containing vacuoles in macrophages

et al. 2018

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“…Moreover, immature neutrophils produced significantly lower levels of ROS in response to PMA and E. coli than mature granulocytes, possibly due to the immaturity of the nicotinamide adenine dinucleotide phosphate oxidase or of the enzymatic pathway of H 2 O 2 production (superoxide dismutase). Interestingly, it was shown that efficiency in bacterial killing was positively correlated with levels in ROS production is septic neutrophils (41). S. aureus induced low levels of H 2 O 2 in neutrophils, and no significant difference was observed between the different neutrophil subsets.…”

Section: Discussionmentioning

confidence: 95%

Innate Immune Functions of Immature Neutrophils in Patients With Sepsis and Severe Systemic Inflammatory Response Syndrome*

Drifte

Dunn-Siegrist

Tissières

et al. 2013

Critical Care Medicine

205

160

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“…Thus, conflicting findings in severe infection could be due to variability in the total numbers of underactive immature neutrophils compared with activated fully-differentiated neutrophils [ 158 , 159 ]. Despite displaying an activated basal state, the mature neutrophils from patients with severe infection do not generate ROS to the same extent as healthy neutrophils following ex vivo stimulation [ 160 ]. The effect of vitamin C supplementation on phagocytosis, oxidant generation, and microbial killing by leukocytes from septic patients has not yet been explored.…”

Section: Vitamin C and Leukocyte Functionmentioning

confidence: 99%

Vitamin C and Immune Function

2017

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Vitamin C is an essential micronutrient for humans, with pleiotropic functions related to its ability to donate electrons. It is a potent antioxidant and a cofactor for a family of biosynthetic and gene regulatory enzymes. Vitamin C contributes to immune defense by supporting various cellular functions of both the innate and adaptive immune system. Vitamin C supports epithelial barrier function against pathogens and promotes the oxidant scavenging activity of the skin, thereby potentially protecting against environmental oxidative stress. Vitamin C accumulates in phagocytic cells, such as neutrophils, and can enhance chemotaxis, phagocytosis, generation of reactive oxygen species, and ultimately microbial killing. It is also needed for apoptosis and clearance of the spent neutrophils from sites of infection by macrophages, thereby decreasing necrosis/NETosis and potential tissue damage. The role of vitamin C in lymphocytes is less clear, but it has been shown to enhance differentiation and proliferation of B- and T-cells, likely due to its gene regulating effects. Vitamin C deficiency results in impaired immunity and higher susceptibility to infections. In turn, infections significantly impact on vitamin C levels due to enhanced inflammation and metabolic requirements. Furthermore, supplementation with vitamin C appears to be able to both prevent and treat respiratory and systemic infections. Prophylactic prevention of infection requires dietary vitamin C intakes that provide at least adequate, if not saturating plasma levels (i.e., 100–200 mg/day), which optimize cell and tissue levels. In contrast, treatment of established infections requires significantly higher (gram) doses of the vitamin to compensate for the increased inflammatory response and metabolic demand.

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Assessment of Neutrophil Function in Patients with Septic Shock: Comparison of Methods

Cited by 10 publications

References 24 publications

The hepcidin-ferroportin axis controls the iron content of Salmonella-containing vacuoles in macrophages

The hepcidin-ferroportin axis controls the iron content of Salmonella-containing vacuoles in macrophages

Innate Immune Functions of Immature Neutrophils in Patients With Sepsis and Severe Systemic Inflammatory Response Syndrome*

Vitamin C and Immune Function

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