Cells and mediators in diisocyanate-induced occupational asthma

Shin, Yoo Seob; Kim, Mi Ae; Pham, Duy Le; Park, Hae‐Sim

doi:10.1097/aci.0b013e32835e0322

Cited by 18 publications

(25 citation statements)

References 87 publications

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“…Although the exact mechanisms are not known, oxidase activity initiates immune activation through its ability to recruit inflammatory cells, including neutrophils. That was the reason for some studies to consider ROS as adjuvants of initiating allergic inflammation [25,31]. By reporting the results of this study, we may propose oxidative stress tests as diagnostic biomarkers for TDI induced asthma as well.…”

Section: Discussionmentioning

confidence: 65%

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Vitamin E Effect in a Rat Model of Toluene Diisocyanate-Induced Asthma

Muti

Pârvu

Muti

et al. 2016

Medicine and Pharmacy Reports

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Background and aimThe aim of the study was to evaluate vitamin E effect upon oxidative stress associated with toluene −2, 4-diisocyanate (TDI)-induced asthma in rats.MethodsThe five study groups were: control, vehicle, TDI, vehicle+E, TDI+E. TDI animals were sensitized by nasal administration of TDI 10% (5μl/nostril) between days 1–7 and 15–21. Between days 22–28 groups TDI+E and vehicle+E rats received vitamin E (50 mg/kg, i. v.), and control, vehicle and TDI groups received saline solution. On day 29 the rats were challenged by intranasal application of 5% TDI (5 μl/nostril). On day 30 blood, BALF and lung biopsy were harvested. Oxidative stress tests were malondialdehyde (MDA), protein carbonyls (PC), total thiols (tSH), 1,1-diphenyl-2-picryl hydrazyl (DPPH) and reduced glutathione (GSH).ResultsTDI sensitization increased oxidative stress systemically, but also locally in the respiratory airways and lung tissue. There was an increase of MDA and PC formation associated with a deficiency of the antioxidant defense reflected by DPPH decreases. There were no differences between systemic and local lung concentrations of oxidized molecules.After vitamin E treatment oxidative stress was reduced mostly due to serum, BALF and lung tissue GSH and DPPH increase.ConclusionThe study showed that in rat TDI-induced asthma there was oxidative stress caused by increased ROS production and antioxidants deficiency, and vitamin E reduced ROS production and improved antioxidant defense.

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Section: Discussionmentioning

confidence: 65%

“…Various kinds of cytokines have an effect on the recruitment of cells that mediate the process of airway inflammation and remodeling [24,25]. …”

Section: Discussionmentioning

confidence: 99%

Vitamin E Effect in a Rat Model of Toluene Diisocyanate-Induced Asthma

Muti

Pârvu

Muti

et al. 2016

Medicine and Pharmacy Reports

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“…As far as we know, plenty of evidence suggested that PI3K signaling plays a pivotal role downstream of oxidative stress in airway inflammation (Marwick et al, 2009) and in pulmonary epithelial cells (Papaiahgari et al, 2006). Oxidative stress was an vitally important mechanism involved in TDI induced asthma (Shin et al, 2013) as well as the most well-established upstream of caspase-1 (Kim et al, 2014). Therefore, it is possible that ROS/PI3K signal pathway mediates TDI induced caspase-1 activation, which deserves our future investigation.…”

Section: Discussionmentioning

confidence: 96%

Phosphatidylinositol 3-kinases pathway mediates lung caspase-1 activation and high mobility group box 1 production in a toluene-diisocyanate induced murine asthma model

et al. 2015

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“…Oxidative stress has been described as a trigger that aids in the development of DI-OA. 8 Moreover, it can aggravate airway inflammation by inducing Abbreviations: AEC, asymptomatic exposed control; DI-OA, diisocyanate-induced occupational asthma; NA, not applicable; NC, normal control; n, number of subjects; q, minor allele frequency. Logistic regression analysis was applied to control for age and sex as covariates.…”

Section: Discussionmentioning

confidence: 99%

“…2,7 Oxidative stress, which plays an important role in the pathogenesis of airway inflammation, has been suggested to be a pathogenic mechanism of DI-OA. 8 It has been demonstrated that inflammation driven by increased oxidative stress occurs in the airways of asthmatic patients. 9 In cases of DI-OA, inhaled DI causes tissue injury, activating both inflammatory and bronchial epithelial cells, which generate reactive oxygen species (ROS) and nitrogen species that cause oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Effects of MBL2 polymorphisms in patients with diisocyanate-induced occupational asthma

et al. 2015

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Diisocyanate (DI) is the most common cause of occupational asthma (OA) in Korea. Mannose-binding lectin (MBL) initiates the lectin complement activation pathway following oxidative stress and plays an important role in the regulation of inflammatory processes. To determine whether there is a genetic association between MBL2 polymorphisms and DI-OA, 99 patients with DI-OA, 99 asymptomatic exposed controls (AECs) and 144 unexposed normal controls were enrolled in this study. Three polymorphisms (−554 G4C, − 431A4C and − 225 G4C) in the MBL2 promoter were genotyped, and serum MBL levels were determined by enzyme-linked immunosorbent assay. Functional variabilities in the promoter polymorphisms were analyzed by a luciferase reporter assay and electrophoretic mobility shift assay (EMSA). A significantly higher frequency of haplotype (ht) 2 [CAG] was noted in the DI-OA group compared with the AEC group (P = 0.044). The patients with DI-OA carrying ht2 [CAG] had significantly lower PC 20 methacholine levels (Po0.001) than the non-carriers. The serum MBL levels were significantly higher in the DI-exposed subjects (both the DI-OA patients and AECs) carrying ht1 [GAG] (P = 0.028). Luciferase activity was significantly enhanced in ht1 [GAG] compared with ht2 [CAG] in human hepatocarcinoma cells (Hep3B) (P = 0.002). The EMSA showed that a − 554G probe produced a specific shifted band compared with the − 554C probe. These findings suggest that decreased serum MBL levels due to polymorphisms of the MBL2 gene may increase susceptibility to the development of DI-OA in DI-exposed individuals.

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Cells and mediators in diisocyanate-induced occupational asthma

Cited by 18 publications

References 87 publications

Vitamin E Effect in a Rat Model of Toluene Diisocyanate-Induced Asthma

Vitamin E Effect in a Rat Model of Toluene Diisocyanate-Induced Asthma

Phosphatidylinositol 3-kinases pathway mediates lung caspase-1 activation and high mobility group box 1 production in a toluene-diisocyanate induced murine asthma model

Effects of MBL2 polymorphisms in patients with diisocyanate-induced occupational asthma

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