Serum specific IgG response to toluene diisocyanate-tissue transglutaminase conjugate in toluene diisocyanate–induced occupational asthmatics

Pham, Duy Le; Kim, Mi-Ae; Yoon, Moon Gyung; Lee, Seung Ihm; Shin, Yoo Seob; Park, Hae‐Sim

doi:10.1016/j.anai.2014.04.022

Cited by 13 publications

(12 citation statements)

References 42 publications

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“…Autoantibodies have been suggested to directly or indirectly (via T cell interactions) induce cytotoxicity, thereby enhancing airway inflammation in SA [ 22 ]. Our group previously detected several autoantibodies, such as anti-CK18, anti-CK19, anti- α -enolase, and tTG antibodies, in the sera of patients with SA [ 10 , 23 – 25 ]. However, the mechanisms underlying autoantibody production in SA are not clear.…”

Section: Discussionmentioning

confidence: 99%

Neutrophil Extracellular DNA Traps Induce Autoantigen Production by Airway Epithelial Cells

Choi

Pham

Lee

et al. 2017

Mediators of Inflammation

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The hypothesis of autoimmune involvement in asthma has received much recent interest. Autoantibodies, such as anti-cytokeratin (CK) 18, anti-CK19, and anti-α-enolase antibodies, react with self-antigens and are found at high levels in the sera of patients with severe asthma (SA). However, the mechanisms underlying autoantibody production in SA have not been fully determined. The present study was conducted to demonstrate that neutrophil extracellular DNA traps (NETs), cytotoxic molecules released from neutrophils, are a key player in the stimulation of airway epithelial cells (AECs) to produce autoantigens. This study showed that NETs significantly increased the intracellular expression of tissue transglutaminase (tTG) but did not affect that of CK18 in AECs. NETs induced the extracellular release of both tTG and CK18 in a concentration-dependent manner. Moreover, NETs directly degraded intracellular α-enolase into small fragments. However, antibodies against neutrophil elastase (NE) or myeloperoxidase (MPO) attenuated the effects of NETs on AECs. Furthermore, each NET isolated from healthy controls (HC), nonsevere asthma (NSA), and SA had different characteristics. Taken together, these findings suggest that AECs exposed to NETs may exhibit higher autoantigen production, especially in SA. Therefore, targeting of NETs may represent a new therapy for neutrophilic asthma with a high level of autoantigens.

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Section: Discussionmentioning

confidence: 99%

Neutrophil Extracellular DNA Traps Induce Autoantigen Production by Airway Epithelial Cells

Choi

Pham

Lee

et al. 2017

Mediators of Inflammation

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“…Recently, it has been demonstrated that PMN have an important role in TDI-induced asthma because they can release ROS having pathological effects on AECs of asthmatic individuals through the oxidative stress16. So, the nonimmune direct oxidative stress effects of diisocyanate may play an important role in the pathogenesis of TDI-induced asthma [26,27]. …”

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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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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“…This study enrolled 137 patients with asthma and 20 healthy controls Atopy was defined as one or more positive reactions on the skin prick test. 23 Serum total IgE levels were measured using the ImmunoCAP system (Thermo Fisher Scientific, Waltham, MA, USA).…”

Section: Study Subjects and Collection Of Clinical Datamentioning

confidence: 99%

Ceramide/sphingosine‐1‐phosphate imbalance is associated with distinct inflammatory phenotypes of uncontrolled asthma

Kim

Jung

Kim

et al. 2020

Allergy

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Background: Asthma is associated with inflammatory dysregulation, but the underlying metabolic signatures are unclear. This study aimed to classify asthma inflammatory phenotypes based on cellular and metabolic features. Methods: To determine cellular and metabolic profiles, we assessed inflammatory cell markers using flow cytometry, sphingolipid (SL) metabolites using LC-MS/MS, and serum cytokines using ELISA. Targeted gene polymorphisms were determined to identify genetic predispositions related to the asthma inflammatory phenotype. Results: In total, 137 patients with asthma and 20 healthy controls (HCs) were enrolled. Distinct cellular and metabolic profiles were found between them; patients with asthma showed increased expressions of inflammatory cell markers and higher levels of SL metabolites compared to HCs (P < .05 for all). Cellular markers (CD66 + neutrophils, platelet-adherent eosinophils) and SL metabolic markers (C16:0 and C24:0 ceramides) for uncontrolled asthma were also identified; higher levels were observed in uncontrolled asthma compared to controlled asthma (P < .05 for all). Asthmatics patients with higher levels of CD66 + neutrophils had lower FEV1(%), higher ACQ (but lower AQLO) scores, and higher sphingosine and C16:0 ceramide levels compared to those with low levels of CD66 + neutrophils. Asthmatics patients with higher levels of platelet-adherent eosinophils had higher S1P levels compared to those with lower levels of platelet-adherent eosinophils. Patients carrying TT genotype of ORMDL3 had more CD66 + neutrophils; those with AG/ GG genotypes of SGMS1 exhibited higher platelet-adherent eosinophils. Conclusion: Patients with uncontrolled asthma possess distinct inflammatory phenotypes including increased CD66 + neutrophils and platelet-adherent eosinophils, with an imbalanced ceramide/S1P rheostat, potentially involving ORMDL3 and SGMS1 gene polymorphisms. Ceramide/S1P synthesis could be targeted to control airway inflammation.

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Serum specific IgG response to toluene diisocyanate-tissue transglutaminase conjugate in toluene diisocyanate–induced occupational asthmatics

Cited by 13 publications

References 42 publications

Neutrophil Extracellular DNA Traps Induce Autoantigen Production by Airway Epithelial Cells

Neutrophil Extracellular DNA Traps Induce Autoantigen Production by Airway Epithelial Cells

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

Ceramide/sphingosine‐1‐phosphate imbalance is associated with distinct inflammatory phenotypes of uncontrolled asthma

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