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Toll-like Receptor 4 Deficiency Aggravates Airway Hyperresponsiveness and Inflammation by Impairing Neutrophil Apoptosis in a Toluene Diisocyanate-Induced Murine Asthma Model.

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Accumulating evidence has suggested that toll-like receptor 4 (TLR4) is critically involved in the pathogenesis of asthma. The aim of this study was to investigate the role of TLR4 in toluene diisocyanate (TDI)-induced allergic airway

Blockade of the NLRP3/Caspase-1 Axis Ameliorates Airway Neutrophilic Inflammation in a Toluene Diisocyanate-Induced Murine Asthma Model.

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Multiple studies have addressed the vital role of Nod-like receptor protein 3(NLRP3)/caspase-1/IL-1β signaling in asthma. Yet, the role of NLRP3/caspase-1 in toluene diisocyanate (TDI)-induced asthma is still obscure. The aim of this study is to investigate the role of the NLRP3/caspase-1 axis in

Effect of long-term exposure to low-level toluene on airway inflammatory response in mice.

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Volatile organic compounds are the main substances causing multiple chemical sensitivity reactions in human. Our laboratory has previously showed that the exposure of low-level formaldehyde causes immunogenic and neurogenic inflammatory responses in mice. The aim of the present study was to

Importance of inflammatory and immune components in a mouse model of airway reactivity to toluene diisocyanate (TDI).

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BACKGROUND Nearly 9 million individuals are exposed to agents in the workplace associated with asthma, and isocyanates represent the most common cause of occupationally induced asthma. OBJECTIVE Nonetheless, the immunological mechanisms responsible for isocyanate-induced asthma are not clear. A

Glutathione-conjugated toluene diisocyanate causes airway inflammation in sensitised mice.

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Toluene diisocyanate (TDI) is a highly volatile compound that reacts readily with nucleophilic compounds, sulfhydryl groups in particular. Since the epithelial lining fluid of the airways contains high levels of the sulfhydryl, glutathione (GSH), inhalation of TDI is likely to result in the

Airway inflammation during late asthmatic reactions induced by toluene diisocyanate.

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To determine the importance of airway inflammation for the development of late asthmatic reactions, we examined sensitized subjects during late asthmatic reactions induced by exposure to toluene diisocyanate (TDI) in the laboratory. Late asthmatic reactions are associated with a transient increase

Effect of Ipomea carnea Jacq. flowers on hematological changes in toluene diisocyanate-induced inflammation in Wistar rats.

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OBJECTIVE To investigate the active chloroform fraction of the ethanol extract of Ipomoea carnea flowers on hematological changes in toluene diisocyanate-induced inflammation in Wistar rats. METHODS Except for the control group, all of the rats were sensitized with intranasal application of 5 μL of

Airway hyperresponsiveness and inflammation induced by toluene diisocyanate in guinea pigs.

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We examined the changes in airway responsiveness to increasing doses of an acetylcholine aerosol in anesthetized and ventilated guinea pigs 2, 6, or 24 h after exposure to 2 ppm toluene diisocyanate (TDI) or 2 h after exposure to air or 1 ppm TDI. Pulmonary resistance (RL) after the animals inhaled

Inflammatory events in the blood and airways of guinea pigs immunized to toluene diisocyanate.

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Toluene diisocyanate (TDI)-induced asthma is a common cause of occupational lung disease. We used a model to investigate the course of bronchopulmonary inflammation following immunization with TDI. Guinea pigs were immunized by weekly intradermal injections and challenged with TDI 7 d after the

Airway inflammation and bronchial remodelling in toluene diisocyanate-exposed BALB/c mouse model.

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Toluene diisocyanate (TDI), a highly reactive industrial chemical, is one of the leading causes of occupation-related asthma in industrialized countries. The pathogenesis of TDI-induced asthma, however, remains not fully understood, in part due to lack of appropriate animal models. Twenty five

Contribution of vascular endothelial growth factor to airway hyperresponsiveness and inflammation in a murine model of toluene diisocyanate-induced asthma.

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Isocyanate chemicals, including toluene diisocyanate (TDI), are currently the most common causes of occupational asthma. Although considerable controversy remains regarding its pathogenesis, TDI-induced asthma is characterized by hyperresponsiveness and inflammation of the airways. One of the

Doxycycline reduces airway inflammation and hyperresponsiveness in a murine model of toluene diisocyanate-induced asthma.

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BACKGROUND Toluene diisocyanate (TDI) is a leading cause of occupational asthma. Although considerable controversy remains regarding its pathogenesis, TDI-induced asthma is an inflammatory disease of the airways characterized by airway remodeling caused, at least in part, by an excess of

Asp-Tyr-Leu-Lys tetrapeptide inhibits airway inflammation in toluene-2,4-diisocyanate-induced asthma mice.

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BACKGROUND Airway inflammation and remodelling contribute to chronic airway obstruction of asthma. Currently, no medication effectively controls airway remodelling and related vascular changes. Therefore, new strategies need to be developed. The kringle 5 domain has anti-angiogenic activity

[Airway inflammatory cell dynamics during late asthmatic reactions induced by toluene diisocyanate in guinea pigs. I. Bronchoalveolar lavage study].

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We developed a guinea pig model of late asthmatic reactions (LAR) induced by toluene diisocyanate (TDI), and investigated airway inflammatory cell dynamics during LAR by bronchoalveolar lavage (BAL) in this model. The guinea pigs were sensitized by nasal application of 10% TDI solution once daily

Thymic stromal lymphopoietin (TSLP) and Toluene-diisocyanate-induced airway inflammation: alleviation by TSLP neutralizing antibody.

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Toluene-diisocyanate (TDI) is mainly used in the manufacturing process of polyurethane foams, and is a potent inducer of occupational asthma characterized by airway inflammation and airway hyperreactivity. Thymic stromal lymphopoietin (TSLP) plays an important role in the development of asthma, and

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