Oxidative inhibition of polymorphonuclear leukocyte motility mediated by the peroxidase/H2O2/halide system: Studies on the reversible nature of the inhibition and mechanism of protection of migratory responsiveness by ascorbate, levamisole, thiamine and cysteine

Jones, Pauline

doi:10.1016/0192-0561(83)90012-7

Cited by 21 publications

(12 citation statements)

References 20 publications

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“…Thiamine is also implicated in the regulation and activation of brain immune cells and the expression of antibodies, immunoglobulins and CD40L‐mediated immune system . Apart from this, thiamine acts as an antioxidant for neutrophil cells, inhibits the reactive oxygen species in macrophages and inhibits p53 during the replication and apoptosis…”

Section: Biochemistry Of Thiamine In Humansmentioning

confidence: 99%

Genetic defects of thiamine transport and metabolism: A review of clinical phenotypes, genetics, and functional studies

Marcé‐Grau

Martí-Sánchez

Baide‐Mairena

et al. 2019

J of Inher Metab Disea

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Thiamine is a crucial cofactor involved in the maintenance of carbohydrate metabolism and participates in multiple cellular metabolic processes within the cytosol, mitochondria, and peroxisomes. Currently, four genetic defects have been described causing impairment of thiamine transport and metabolism: SLC19A2 dysfunction leads to diabetes mellitus, megaloblastic anemia and sensory‐neural hearing loss, whereas SLC19A3, SLC25A19, and TPK1‐related disorders result in recurrent encephalopathy, basal ganglia necrosis, generalized dystonia, severe disability, and early death. In order to achieve early diagnosis and treatment, biomarkers play an important role. SLC19A3 patients present a profound decrease of free‐thiamine in cerebrospinal fluid (CSF) and fibroblasts. TPK1 patients show decreased concentrations of thiamine pyrophosphate in blood and muscle. Thiamine supplementation has been shown to improve diabetes and anemia control in Rogers' syndrome patients due to SLC19A2 deficiency. In a significant number of patients with SLC19A3, thiamine improves clinical outcome and survival, and prevents further metabolic crisis. In SLC25A19 and TPK1 defects, thiamine has also led to clinical stabilization in single cases. Moreover, thiamine supplementation leads to normal concentrations of free‐thiamine in the CSF of SLC19A3 patients. Herein, we present a literature review of the current knowledge of the disease including related clinical phenotypes, treatment approaches, update of pathogenic variants, as well as in vitro and in vivo functional models that provide pathogenic evidence and propose mechanisms for thiamine deficiency in humans.

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Section: Biochemistry Of Thiamine In Humansmentioning

confidence: 99%

Genetic defects of thiamine transport and metabolism: A review of clinical phenotypes, genetics, and functional studies

Marcé‐Grau

Martí-Sánchez

Baide‐Mairena

et al. 2019

J of Inher Metab Disea

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“…Thiamine deficiency in a mouse model showed a high level of 4-hydroxy 2-nonenal (4-HNE), a product of ROS-induced lipid peroxidation in the cell membrane [47]. The actions of vitamin B1 also prevent the PMN motility-inhibiting effects of the horseradish peroxidase (HRP)/H 2 O 2 /halide system and protect the neutrophil sulfhydryl groups, an indicator of the state of reduction of the cell [48]. We established that vitamin B1 treatment at concentrations of 5 and 15 mg/ml in human PMNs in vitro showed significantly decreased ROS generation, leading to the inhibitory action in PMA or S .…”

Section: Discussionmentioning

confidence: 99%

Transketolase and vitamin B1 influence on ROS-dependent neutrophil extracellular traps (NETs) formation

et al. 2019

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Neutrophil extracellular traps (NETs) are a recently identified, web-like, extracellular structure composed of decondensed nuclear DNA and associated antimicrobial granules. NETs are extruded into the extracellular environment via the reactive oxygen species (ROS)-dependent cell death pathway participating in inflammation and autoimmune diseases. Transketolase (TKT) is a thiamine pyrophosphate (vitamin B1)-dependent enzyme that links the pentose phosphate pathway with the glycolytic pathway by feeding excess sugar phosphates into the main carbohydrate metabolic pathways to generate biosynthetic reducing capacity in the form of NADPH as a substrate for ROS generation. In this work, TKT was selected as a lead candidate from 24 NET-associated proteins obtained by literature screening and knowledge gap assessment. Consequently, we determined whether TKT influenced NET formation in vitro . We firstly established that the release of ROS-dependent NETs was significantly decreased after purified human PMNs were pretreated with oxythiamine, a TKT inhibitor, and in a concentration dependent manner. As a cofactor for TKT reaction, we evaluated the release of NET formation either in vitamin B1 treatment or in combined use of oxythiamine and vitamin B1, and found that those treatments also exerted a significant suppressive effect on the amount of NET-DNA and ROS production. The regulation of TKT by oxythiamine and/or vitamin B1 may therefore be associated with response to the modulation of NET formation by preventing generation of excessive NETs in inflammatory diseases.

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“…They concluded from the observed chemotaxis-enhancing effects of mannitol and dimethylsulfoxide and the iron chelator desferal that hydroxyl radicals were responsible for PMN autooxidation during che motactic migration. Again it is strange that SOD, which removes the First product of oxygen reduction from which all the others are derived, should be with out effect [5], A motility-inhibiting effect on PMN was also observed with the added combination of HPO-H20 2-Nal [27], In contrast, Flohe et al [6] observed decreased che motactic migration of human PMN in Boyden cham bers towards LTB4, FMLP and C5a in the presence of SOD, suggesting that some ROM species was re quired for chemotaxis. Kato et al [28] also reported a partial suppression by SOD of human PMN chemo taxis towards FMLP.…”

Section: Discussionmentioning

confidence: 99%

Production of Superoxide Anion and Hydrogen Peroxide by Human Neutrophilic Granulocytes during Chemotactic Migration towards f-Met-Leu-Phe, C5a, Leukotriene B4, Monocyte-Derived Chemotaxin/IL-8 and Platelet-Activating Factor

Kownatzki

Uhrich

1990

Int Arch Allergy Immunol

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During the chemotactic migration of human neutrophilic granulocytes towards the chemotactic factors f-Met-Leu-Phe, C5a, leukotriene B₄ (LTB₄), monocyte-derived chemotaxin (MOC/IL-8) and platelet-activating factor (PAF) in Boyden chambers, the production of superoxide anion and hydrogen peroxide was measured by superoxide dismutase-inhibitable cytochrome C reduction and oxidation of p-OH-phenylacetic acid, respectively. With the exception of 10^––⁶M PAF, none of the factors at optimal chemotactic concentrations induced the production of O₂ or H₂O₂ in amounts significantly different from neutrophilic granulocytes migrating at random. At 20–50 times the optimal chemotactic concentration some O₂ and H₂O₂ production was observed with f-Met-Leu-Phe, C5a and LTB₄, but not with MOC/IL-8. Superoxide dismutase, catalase or a combination of the two added to both compartments of the Boyden chambers did not affect the random or chemotactic migration towards any of the chemotactic factors. The results suggest that chemotactic migration and the production of reactive oxygen metabolites by human neutrophilic granulocytes are unrelated events.

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Oxidative inhibition of polymorphonuclear leukocyte motility mediated by the peroxidase/H2O2/halide system: Studies on the reversible nature of the inhibition and mechanism of protection of migratory responsiveness by ascorbate, levamisole, thiamine and cysteine

Cited by 21 publications

References 20 publications

Genetic defects of thiamine transport and metabolism: A review of clinical phenotypes, genetics, and functional studies

Genetic defects of thiamine transport and metabolism: A review of clinical phenotypes, genetics, and functional studies

Transketolase and vitamin B1 influence on ROS-dependent neutrophil extracellular traps (NETs) formation

Production of Superoxide Anion and Hydrogen Peroxide by Human Neutrophilic Granulocytes during Chemotactic Migration towards f-Met-Leu-Phe, C5a, Leukotriene B4, Monocyte-Derived Chemotaxin/IL-8 and Platelet-Activating Factor

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