Redox regulation of mast cell histamine release in thioredoxin-1 (TRX) transgenic mice

Son, Aoi; Nakamura, Hajime; Kondo, Norihiko; Matsuo, Yoshiyuki; Liu, Wenrui; Oka, Shinichi; Ishii, Yasuyuki; Yodoi, Junji

doi:10.1038/sj.cr.7310031

Cited by 35 publications

(22 citation statements)

References 48 publications

(38 reference statements)

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“…Reduction of 5-LO activity by the PHGP mimetic ebselen (22,33) or using specific 5-LO and COX-1 inhibitors (53) has minimal effects on mast cell degranulation. In another study using mBMMC deficient in the antioxidant enzyme thioredoxin, Ag mediated degranulation was reduced compared with WT mBMMC (54). These data appear to contradict our current data on degranulation and may involve differences in localization of the antioxidant enzyme.…”

Section: Discussioncontrasting

confidence: 55%

FcεRI- and Fcγ Receptor-Mediated Production of Reactive Oxygen Species by Mast Cells Is Lipoxygenase- and Cyclooxygenase-Dependent and NADPH Oxidase-Independent

Swindle

Coleman

DeLeo

et al. 2007

The Journal of Immunology

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We investigated the enzymes responsible for FcεRI-dependent production of reactive oxygen species (ROS) and the influence of ROS on mast cell secretory responses. 5-Lipoxygenase (5-LO) was the primary enzyme involved in ROS production by human mast cells (huMC) and mouse bone marrow-derived mast cells (mBMMC) following FcεRI aggregation because incubation with 5-LO inhibitors (AA861, nordihydroguaiaretic acid, zileuton) but not a flavoenzyme inhibitor (diphenyleneiodonium) completely abrogated Ag-induced dichlorodihydrofluorescein (DCF) fluorescence. Furthermore, 5-LO-deficient mBMMC had greatly reduced FcεRI-dependent DCF fluorescence compared with wild type mBMMC or those lacking a functional NADPH oxidase (i.e., gp91phox- or p47phox-deficient cells). A minor role for cyclooxygenase (COX)-1 in FcεRI-dependent ROS production was demonstrated by inhibition of Ag-mediated DCF fluorescence by a COX-1 inhibitor (FR122047) and reduced DCF fluorescence in COX-1-deficient mBMMC. Complete abrogation of FcεRI-dependent ROS production in mast cells had no effect on degranulation or cytokine secretion. In response to the NADPH oxidase-stimulating agents including PMA, mBMMC and huMC produced negligible ROS. IgG-coated latex beads did stimulate ROS production in huMC, and in this experiment 5-LO and COX again appeared to be the enzymatic sources of ROS. In contrast, IgG-coated latex bead-induced ROS production in human polymorphonuclear leukocytes occurred by the NADPH oxidase pathway. Thus mBMMC and huMC generate ROS by 5-LO and COX-1 in response to FcεRI aggregation; huMC generate ROS upon exposure to IgG-coated latex beads by 5-LO and COX; and ROS appear to have no significant role in FcεRI-dependent degranulation and cytokine production.

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Section: Discussioncontrasting

confidence: 55%

FcεRI- and Fcγ Receptor-Mediated Production of Reactive Oxygen Species by Mast Cells Is Lipoxygenase- and Cyclooxygenase-Dependent and NADPH Oxidase-Independent

Swindle

Coleman

DeLeo

et al. 2007

The Journal of Immunology

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“…By contrast, in a mouse model of inflammatory bowel disease, TRX-Tg mice produced lower levels of IFN-g and TNF-a compared with WT mice [32]. It also has been shown that Ag-specific IgG1 responses were increased in TRX-Tg mice with associated decreases in Ag-specific IgG2a levels and IFN-g mRNA expression in the spleen [33]. Comparisons between these studies are complicated, however, because there are variations in mouse genetic background and/or immunization protocol (Ag, adjuvant, and route) used in these studies.…”

Section: Discussionmentioning

confidence: 98%

Thioredoxin suppresses airway inflammation independently of systemic Th1/Th2 immune modulation

Torii

Wang

et al. 2010

Eur J Immunol

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Oxidative stress plays an important role in the pathogenesis of asthma via the upregulation of local inflammatory mediators and/or promoting Th2-skewing during Ag sensitization. Thioredoxin (TRX), a 12 kDa redox-active protein with antioxidative property, has been recently shown to play a protective role in various inflammatory diseases. Using a mouse model of asthma, we show here that IL-13 and eotaxin production are decreased in TRX-Tg mice leading to reduced eosinophils recruitment and mucus metaplasia. The reduction in airway inflammation occurs without the attenuation of systemic Th2 immunity in that comparable levels of Th2-type cytokines and Ig were detected in LN and serum, respectively, from TRX-Tg and WT mice. Likewise, CD4 1 T cells from both strains of mice developed similar Th1 and Th2 responses in vitro. Asthmatic lungs of TRX-Tg and WT mice contained similar amounts of GATA-3 1 and Foxp3 1 T cells. Finally, production of MIF, an upstream modulator of airway inflammation, was significantly reduced in the lungs of TRX-Tg mice. Our data suggest that TRX suppresses airway inflammation by inhibiting MIF production thereby limiting the downstream recruitment of eosinophils to the lung independently of modulating systemic Th1/Th2 immunity.

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“…Dietary Se levels have been shown to affect TR-1 activity and TRX levels in a wide range of tissues [32]. Several experiments have utilized a mouse model involving a transgenic mouse overexpressing human TRX (TRX-Tg) or treatment with recombinant TRX to show that increased abundance of this important reducing compound is effective in reducing inflammation during a wide range of immunological processes, including experimental colitis, LPS-induced bronchoalveolar neutrophil infiltration, myosin-induced autoimmune myocarditis, mast cell degranulation, and asthma development [39,53,77,80,81]. Part of the mechanism by which TRX carries out anti-inflammatory effects is through altered levels of certain cytokines and eicosinoids.…”

Section: Trx Reductase Balances Redox and Inflammationmentioning

confidence: 99%

Mechanisms by which selenium influences immune responses

Hoffmann

2007

Arch. Immunol. Ther. Exp.

121

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Selenium (Se) is an essential dietary trace element that influences immune responses through its incorporation into selenoproteins as the amino acid selenocysteine. This review summarizes data available to date regarding the mechanisms by which Se exerts its effects on inflammation and immune responses. This includes the effects of Se on phagocytes as well as effects on lymphocyte activation, proliferation, and differentiation. Also examined are the known functions of individual selenoproteins for regulating reactive oxygen species and redox potential in leukocytes. Overall, determining how Se contributes to optimal immune responses will depend on a better understanding of the mechanisms by which the selenoproteins, individually and collectively, shape inflammation and immune responses.

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Redox regulation of mast cell histamine release in thioredoxin-1 (TRX) transgenic mice

Cited by 35 publications

References 48 publications

FcεRI- and Fcγ Receptor-Mediated Production of Reactive Oxygen Species by Mast Cells Is Lipoxygenase- and Cyclooxygenase-Dependent and NADPH Oxidase-Independent

FcεRI- and Fcγ Receptor-Mediated Production of Reactive Oxygen Species by Mast Cells Is Lipoxygenase- and Cyclooxygenase-Dependent and NADPH Oxidase-Independent

Thioredoxin suppresses airway inflammation independently of systemic Th1/Th2 immune modulation

Mechanisms by which selenium influences immune responses

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