Molecular basis of chronic granulomatous disease [see comments]

Rm, Smith; Curnutte, JT

doi:10.1182/blood.v77.4.673.bloodjournal774673

Cited by 101 publications

(21 citation statements)

References 96 publications

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“…We show that myeloid cells from CGD patients are relatively resistant to the growth-inhibitory action mediated by TNJ?. CGD is a congenital disorder in which phagocytes cannot generate superoxide because of deficiency in any one of at least four components of the superoxide-generating enzyme, NADPH oxidase (Curnutte et al, 1974(Curnutte et al, , 1975Hohn & Lehrer, 1975: Smith & Curnutte, 1991. Pioneering studies in a number of laboratories demonstrated that NADPH oxidase was inactive in unstiiulated celks; but when the cells were stimulated the enzyme was located exclusively on the cellular plasma membrane (Briggs et al, 1977: Dewald et al, 1978.…”

Section: Discussionmentioning

confidence: 99%

“…CGD is caused by a defect in any one of four NADPH oxidase components, gp91-phox. p22-phox, p47-phox and p67-phox (Smith & Curnutte, 1991). We present evidence that cytotoxicity of TNF is mediated, at least in part, through production of superoxide, and haemopoietic cells from CGD patients are relatively resistant to the growth inhibitory action of TNF.…”

mentioning

confidence: 80%

“…Chronic granulomatous disease (CGD) is a congenital disorder in which phagocytes cannot generate superoxide (Curnutte et al, 1974(Curnutte et al, , 1975(Curnutte et al, . 1988(Curnutte et al, , 1989Hohn & Lehrer, 1975;Smith & Curnutte, 1991;Briggs et al, 1977;Dewald et al 1978;Parkos et al 1987Parkos et al , 1988Clark et al, 1990;Heyworth et al, 1991). CGD is caused by a defect in any one of four NADPH oxidase components, gp91-phox.…”

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confidence: 99%

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Myeloid haemopoietic cells of patients with chronic granulomatous disease are relatively resistant to TNF

Sakashita¹,

Curnutte²,

Koeffler³

1994

Br J Haematol

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Generation of superoxide may be a key step in the cytotoxicity mediated by tumour necrosis factor (TNF); cells that cannot produce oxygen radicals might be resistant to TNF. Myeloid haemopoietic cells from patients with chronic granulomatous disease (CGD) cannot produce a large burst of oxygen radicals; therefore we examined the ability of TNF to inhibit clonal growth of myeloid haemopoietic cells from patients and carriers with several types of CGD. Mononuclear light-density cells from the peripheral blood of 13 CGD patients (11 patients with defects of gp91-phox and two with p47-phox), five gp91-phox carriers and 10 normal volunteers were cultured with the appropriate growth factor and TNF in methylcellulose. As expected, TNF (0.001-100 ng/ml) inhibited colony formation of myeloid cells of normal volunteers in a dose-dependent manner. In contrast, clonal growth of myeloid cells of CGD patients was resistant to inhibition by TNF < or = 100 ng/ml. As expected, the effects of TNF on erythroid clonogenic cells, which are not capable of producing an oxygen burst, and the action of TGF-beta on clonal growth of myeloid cells, were similar in both the individuals with CGD and the normal volunteers. In X chromosome-linked female carriers of CGD (gp91-phox deficiency), TNF showed an intermediate cytotoxicity on clonal growth of myeloid cells, and analysis of NBT reduction demonstrated that the colonies derived from myeloid cells deficient in gp91-phox were resistant to TNF and those derived from the myeloid cells expressing gp91-phox were inhibited in their proliferation by TNF. This study shows for the first time that myeloid haemopoietic cells from patients with CGD are relatively resistant to the growth-inhibiting effects of high concentrations of TNF.

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Section: Discussionmentioning

confidence: 99%

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confidence: 80%

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confidence: 99%

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Myeloid haemopoietic cells of patients with chronic granulomatous disease are relatively resistant to TNF

Sakashita¹,

Curnutte²,

Koeffler³

1994

Br J Haematol

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“…The effects of OxPAPC on oxidative burst are important in the context of infectious diseases as oxidative burst is crucial for optimal bacterial killing [4]. Indeed, patients with defects in the NADPH oxidase complex, exhibit chronic granulomatous disease (CGD), which is associated with recurrent bacterial and fungal infections [54].…”

Section: Effects Of Oxpl On Cell Signaling and Function In The Contexmentioning

confidence: 99%

Accumulating evidence for a role of oxidized phospholipids in infectious diseases

Matt

Sharif

Martins

et al. 2014

Cell. Mol. Life Sci.

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Oxidized phospholipids (OxPL) were originally discovered as by-products and mediators of chronic inflammation such as in atherosclerosis. Over the last years, an increasing body of evidence led to the notion that OxPL not only contribute to the pathogenesis of chronic inflammatory processes but in addition play an integral role as modulators of inflammation during acute infections. Thereby, host defense mechanisms involve the generation of oxygen radicals that oxidize ubiquitously present phospholipids, which in turn act as danger-associated molecular patterns (DAMPs). These OxPL-derived DAMPs can exhibit both pro- and anti-inflammatory functions that ultimately alter the host response to pathogens. In this review, we summarize the currently available data on the role of OxPL in infectious diseases.

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“…This non-mitochondrial O 2 consumption process is known as the respiratory burst. Reactive O 2 species produced during the respiratory burst are believed to serve as bactericidal agents, as evinced by the susceptibility of patients with chronic granulomatous disease to serve recurrent infections (Smith & Curnutte, 1991). Under certain circumstances, the excessive or inappropriate release of these highly reactive O 2 species can result in undesirable tissue damage.…”

Section: Introductionmentioning

confidence: 99%

Cellular localization of the inhibitory action of abruquinone A against respiratory burst in rat neutrophils

Hsu

Raung

Tsao

et al. 1997

British J Pharmacology

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1 The possible mechanisms of action of the inhibitory eect of abruquinone A on the respiratory burst in rat neutrophils in vitro was investigated. 2 Abruquinone A caused an irreversible and a concentration-dependent inhibition of formylmethionylleucyl-phenylalanine (fMLP) plus dihydrocytochalasin B (CB)-and phorbol 12-myristate 13-acetate (PMA)-induced superoxide anion (O 2 . 5 Abruquinone A did not aect the enzyme activities of neutrophil cytosolic protein kinase C (PKC) and porcine heart protein kinase A (PKA). 6 Abruquinone A had no eect on intracellular guanosine 3' : 5'-cyclic monophosphate (cyclic GMP) levels but decreased the adenosine 3' : 5'-cyclic monophosphate (cyclic AMP) levels. 7 The cellular formation of phosphatidic acid (PA) and phosphatidylethanol (PEt) induced by fMLP/ CB was inhibited by abruquinone A with IC 50 values of 2.2+0.6 mg ml 71 and 2.5+0.3 mg ml 71 , respectively. Abruquinone A did not inhibit the fMLP/CB-induced protein tyrosine phosphorylation but induced additional phosphotyrosine accumulation on proteins of 73 ± 78 kDa in activated neutrophils. 8 Abruquinone A inhibited both the O 2. 7 generation in PMA-activated neutrophil particulate NADPH oxidase (IC 50 0.6+0.1 mg ml 71) and the iodonitrotetrazolium violet (INT) reduction in arachidonic acid (AA)-activated cell-free system (IC 50 1.5+0.2 mg ml 71 ). 9 Collectively, these results indicate that the inhibition of respiratory burst in rat neutrophils by abruquinone A is mediated partly by the blockade of phospholipase C (PLC) and phospholipase D (PLD) pathways, and by suppressing the function of NADPH oxidase through the interruption of electron transport.

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Molecular basis of chronic granulomatous disease [see comments]

Cited by 101 publications

References 96 publications

Myeloid haemopoietic cells of patients with chronic granulomatous disease are relatively resistant to TNF

Myeloid haemopoietic cells of patients with chronic granulomatous disease are relatively resistant to TNF

Accumulating evidence for a role of oxidized phospholipids in infectious diseases

Cellular localization of the inhibitory action of abruquinone A against respiratory burst in rat neutrophils

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