Neutrophils cause oxidative DNA damage in alveolar epithelial cells

Knaapen, Ad M.; Seiler, Frank; Schilderman, P.A.E.L.; Nehls, Peter; Bruch, Joachim; Schins, Roel P. F.; Borm, Paul J. A.

doi:10.1016/s0891-5849(98)00285-8

Cited by 125 publications

(71 citation statements)

References 26 publications

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“…phagocytosis and killing of bacteria. After phagocytosis, these cells release large amounts of cytotoxic free radicals and pro-inflammatory cytokine in order to destroy fagocytized bacteria (Knaapen et al, 1999). Inflammatory substances resulting from the release of highly reactive molecules mitigate antioxidants which are intracellular defense mechanisms against oxidation.…”

Section: Resultsmentioning

confidence: 99%

Influence of blood serum selenium on udder health in dairy cows

et al. 2014

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The aim of this study was to determine the effect of selenium concentration in early lactation on mammary gland health and histological characteristics of the udder. The experiment included 30 high-yielding Holstein-Friesian cows. Selenium concentrations in blood and milk serum, and the average somatic cell count in the first and sixth months of lactation were analyzed. After exclusion of the experimental cows from the herd, histological characteristics of the udder were examined (the degree of leukocyte infiltration and the number of granulomas in the parenchyma). The mean selenium concentration in the blood serum was 0.62±0.11 mmol/L and that in the milk serum was 0.12±0.07 mmol/L. Optimal blood levels of selenium were found in 19 cows and suboptimal levels in 11 cows. A significant negative correlation was observed between blood and milk selenium concentrations and somatic cell count in early and mid lactation. There was no relationship between blood selenium concentration, milk selenium concentration and the amount of milk produced. Selenium-deficient cows had a significantly higher milk somatic cell count in early and mid lactation and significantly lower levels of selenium in milk. Upon histological analysis, 120 samples of individual quarters of the udder were grouped according to the degree of leukocyte infiltration and number of granulomas. Results showed that an increase in the degree of leukocyte infiltration and number of granulomas leads to an increase in the proportion of quarters from selenium-deficient cows and a decline in the percentage of quarters from cows exhibiting normal blood selenium concentrations. Selenium has a significant impact on udder health. Changes caused by selenium deficiency occur due to marked inflammation process in the mammary gland.

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Section: Resultsmentioning

confidence: 99%

Influence of blood serum selenium on udder health in dairy cows

et al. 2014

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“…Longstanding observations have confirmed a contributory role of oxygen radicals to the etiology of chronic lung inflammation in both the adult and neonatal populations (6,38 -40). Furthermore, oxygen radicals have been shown to mediate DNA damage (44), an important mechanism of lung injury (45,46). PMN are not the sole source of ROI; other leukocytes, as well as the lung microenvironment itself, can potentially elaborate …”

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confidence: 99%

Neonatal Neutrophils with Prolonged Survival Exhibit Enhanced Inflammatory and Cytotoxic Responsiveness

et al. 2005

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Apoptosis is critical to the resolution of inflammation, as it promotes the removal of neutrophils (PMN) by the reticuloendothelial system. In contrast, PMN persistence characterizes the early stages of chronic inflammation. Adult PMN with delayed senescence retain some functionality, although this has not been described for neonatal PMN. We hypothesized that neonatal PMN with prolonged survival retain cytotoxic and inflammatory function. To test one aspect of inflammatory function, we determined surface CD11b expression on 0-h and 24-h PMN after chemotactic formyl-methionine-leucine-phenylalanine (fMLP) stimulation. Although fMLP induced a greater percentage upregulation of CD11b on 0-h adult PMN, this was similar between nonapoptotic cord blood and adult PMN at 24 h. Furthermore, percentage up-regulation of CD11b was more robust for 24-h than for 0-h cord blood PMN. In contrast, there was no difference in responsiveness between 0-h and 24-h adult PMN. In studies of cytotoxic potential, we determined the expression of reactive oxygen intermediates (ROI) in phorbol 12-myristate 13-acetatestimulated cord blood and adult PMN at 0 h and in 24-h nonapoptotic PMN, using the dihydrorhodamine 123 assay.Stimulated cord blood PMN generated more ROI than did adult PMN at both 0 h and 24 h; in addition, ROI levels in 24-h cord blood PMN were similar to those of 0-h adult PMN. We conclude that PMN with prolonged survival retain specific cytotoxic and inflammatory functions, and these are enhanced in cord blood PMN. We speculate that neonatal PMN with prolonged survival have the functional capacity to contribute to the pathogenesis of inflammatory disorders. Abbreviations CLD, chronic lung disease DHR, dihydrorhodamine 123 fMLP, formyl-methionine-leucine-phenylalanine PE, phycoerythrin PMA, phorbol 12-myristate 13-acetate PMN, neutrophil(s) ROI, reactive oxygen intermediates 7-AAD, 7-aminoactinomycin PMN serve as the primary line of host defense during the early stages of sepsis and inflammation (1). After activation by systemic or local factors, primed endothelial cells interact with PMN through adhesion molecules that include selectins and integrins (2). These adhesive interactions initiate a process that allows the extravasation of PMN into inflamed tissue with the goal of neutralizing the inciting stimulus. In the case of inflammation mediated by bacterial or fungal microorganisms, phagocytosis and subsequent killing of these invaders occurs through mechanisms that partly involve ROI and proteases (3,4).The concept that apoptosis of inflammatory PMN and their timely removal by resident macrophages are critical to the resolution of inflammation has been well established (5,6). During the resolution phase, PMN typically undergo the phenotypic changes associated with apoptosis, which promotes their removal by resident macrophages (7). PMN can also undergo necrosis and lysis, a process that induces cytotoxicity in surrounding tissues (8), although apoptosis is the more common and physiologically preferable route. All cells a...

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“…In lung epithelial cells, oxidative damage to DNA is caused not only by air pollutants, but also by neutrophil products [19]. Using high-density DNA microarrays, lung epithelial cells exposed to oxidative injury showed early induction of bcl-2 and mdm-2, genes which are known to be are involved in the regulation of apoptosis [20].…”

Section: Discussionmentioning

confidence: 99%

Dissociation of DNA damage and mitochondrial injury caused by hydrogen peroxide in SV-40 transformed lung epithelial cells

et al. 2002

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BackgroundSince lung epithelial cells are constantly being exposed to reactive oxygen intermediates (ROIs), the alveolar surface is a major site of oxidative stress, and each cell type may respond differently to oxidative stress. We compared the extent of oxidative DNA damage with that of mitochondrial injury in lung epithelial cells at the single cell level.ResultDNA damage and mitochondrial injury were measured after oxidative stress in the SV-40 transformed lung epithelial cell line challenged with hydrogen peroxide (H2O2). Single cell analysis of DNA damage was determined by assessing the number of 8-oxo-2-deoxyguanosine (8-oxo-dG) positive cells, a marker of DNA modification, and the length of a comet tail. Mitochondrial membrane potential, ΔΨm, was determined using JC-1. A 1 h pulse of H2O2 induced small amounts of apoptosis (3%). 8-oxo-dG-positive cells and the length of the comet tail increased within 1 h of exposure to H2O2. The number of cells with reduced ΔΨm increased after the addition of H2O2 in a concentration-dependent manner. In spite of a continual loss of ΔΨm, DNA fragmentation was reduced 2 h after exposure to H2O2.ConclusionThe data suggest that SV-40 transformed lung epithelial cells are resistant to oxidative stress, showing that DNA damage can be dissociated from mitochondrial injury.

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Neutrophils cause oxidative DNA damage in alveolar epithelial cells

Cited by 125 publications

References 26 publications

Influence of blood serum selenium on udder health in dairy cows

Influence of blood serum selenium on udder health in dairy cows

Neonatal Neutrophils with Prolonged Survival Exhibit Enhanced Inflammatory and Cytotoxic Responsiveness

Dissociation of DNA damage and mitochondrial injury caused by hydrogen peroxide in SV-40 transformed lung epithelial cells

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