chlorine/inflammation

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Inhalation of chlorine causes long-standing lung inflammation and airway hyperresponsiveness in a murine model of chemical-induced lung injury.

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Chlorine is highly irritating when inhaled, and is a common toxic industrial gas causing tissue damage in the airways followed by an acute inflammatory response. In this study, we investigated mechanisms by which chlorine exposure may cause reactive airways dysfunction syndrome (RADS) and we

Upregulation of autophagy decreases chlorine-induced mitochondrial injury and lung inflammation.

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The mechanisms of toxicity during exposure of the airways to chlorinated biomolecules generated during the course of inflammation and to chlorine (Cl2) gas are poorly understood. We hypothesized that lung epithelial cell mitochondria are damaged by Cl2 exposure and activation of autophagy mitigates

Acute respiratory changes and pulmonary inflammation involving a pathway of TGF-β1 induction in a rat model of chlorine-induced lung injury.

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We investigated acute and delayed respiratory changes after inhalation exposure to chlorine (Cl2) with the aim to understand the pathogenesis of the long-term sequelae of Cl2-induced lung-injury. In a rat model of nose-only exposure we analyzed changes in airway hyperresponsiveness (AHR),

Montelukast reduces inhaled chlorine triggered airway hyperresponsiveness and airway inflammation in the mouse.

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OBJECTIVE Cysteinyl leukotrienes (CysLTs) are pro-inflammatory lipid mediators that exacerbate disease state in several asthma phenotypes including asthma induced by allergen, virus and exercise. However, the role of CysLTs in irritant-induced airway disease is not well characterized. The purpose of

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11cintermediate macrophages.

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BACKGROUND

Chlorine is widely used in daily life as disinfectant. However, chronic exposure to chlorine products aggravates allergic T_H 2 inflammation and airway hyperresponsiveness (AHR). Innate lymphoid cells (ILCs) in airways contribute to the inception of asthma in

Anti-inflammatory drugs degradation during LED-UV ₃₆₅ photolysis of free chlorine: roles of reactive oxidative species and formation of disinfection by-products

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Light-emitting diode (LED) is environmentally friendly with longer life compared with traditionally mercury lamps. This study investigated the non-steroidal anti-inflammatory drugs (NSAIDs)- phenacetin (PNT) and acetaminophen (ACT)- removal during LED-UV (365 nm) photolysis of free available

Nasal inflammatory and respiratory parameters in human volunteers during and after repeated exposure to chlorine.

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The objectives of this study were: 1) to determine if chlorine exposure at low levels induces nasal effects in humans as it does in rodents; and 2) to establish a possible occurrence of respiratory effects in human volunteers exposed to chlorine vapour at concentrations of 0, 0.1, 0.3 and 0.5 ppm.

Detection, transformation, and toxicity of indole-derivative nonsteroidal anti-inflammatory drugs during chlorine disinfection

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As important emerging contaminants, nonsteroidal anti-inflammatory drugs (NSAIDs) are the most intensively prescribed pharmaceuticals introduced to drinking water due to their incomplete removal in wastewater treatment. While concentrations of NSAIDs in drinking water are generally low, they have

Inhibition of chlorine-induced pulmonary inflammation and edema by mometasone and budesonide.

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Chlorine gas is a widely used industrial compound that is highly toxic by inhalation and is considered a chemical threat agent. Inhalation of high levels of chlorine results in acute lung injury characterized by pneumonitis, pulmonary edema, and decrements in lung function. Because inflammatory

Early treatment of chlorine-induced airway hyperresponsiveness and inflammation with corticosteroids.

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Chlorine (Cl2) is an industrial gas that is highly toxic and irritating when inhaled causing tissue damage and an acute inflammatory response in the airways followed by a long-term airway dysfunction. The aim of this study was to evaluate whether early anti-inflammatory treatment can protect against

Inflammation and airway hyperresponsiveness after chlorine exposure are prolonged by Nrf2 deficiency in mice.

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Chlorine gas (Cl2) is a potent oxidant and trigger of irritant induced asthma. We explored NF-E2-related factor 2 (Nrf2)-dependent mechanisms in the asthmatic response to Cl2, using Nrf2-deficient mice, buthionine sulfoximine (BSO), an inhibitor of glutathione (GSH) synthesis and sulforaphane (SFN),

Acute chlorine gas exposure produces transient inflammation and a progressive alteration in surfactant composition with accompanying mechanical dysfunction.

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Acute Cl2 exposure following industrial accidents or military/terrorist activity causes pulmonary injury and severe acute respiratory distress. Prior studies suggest that antioxidant depletion is important in producing dysfunction, however a pathophysiologic mechanism has not been elucidated. We

Abnormal epithelial structure and chronic lung inflammation after repair of chlorine-induced airway injury.

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Chlorine is a toxic gas used in a variety of industrial processes and is considered a chemical threat agent. High-level chlorine exposure causes acute lung injury, but the long-term effects of acute chlorine exposure are unclear. Here we characterized chronic pulmonary changes following acute

Chlorination of pyridinium compounds. Possible role of hypochlorite, N-chloramines, and chlorine in the oxidation of pyridinoline cross-links of articular cartilage collagen type II during acute inflammation.

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Reactive oxygen species produced by activated neutrophils and monocytes are thought to be involved in mediating the loss of collagen and other matrix proteins at sites of inflammation. To evaluate their potential to oxidize the pyridinoline (Pyd) cross-links found in collagen types I and II, we

[New chlorine derivatives of indole-3-acetic acid and their effect on experiments inflammation. I].

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chlorine/inflammation

Inhalation of chlorine causes long-standing lung inflammation and airway hyperresponsiveness in a murine model of chemical-induced lung injury.

Upregulation of autophagy decreases chlorine-induced mitochondrial injury and lung inflammation.

Acute respiratory changes and pulmonary inflammation involving a pathway of TGF-β1 induction in a rat model of chlorine-induced lung injury.

Montelukast reduces inhaled chlorine triggered airway hyperresponsiveness and airway inflammation in the mouse.

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11cintermediate macrophages.

Anti-inflammatory drugs degradation during LED-UV 365 photolysis of free chlorine: roles of reactive oxidative species and formation of disinfection by-products

Nasal inflammatory and respiratory parameters in human volunteers during and after repeated exposure to chlorine.

Detection, transformation, and toxicity of indole-derivative nonsteroidal anti-inflammatory drugs during chlorine disinfection

Inhibition of chlorine-induced pulmonary inflammation and edema by mometasone and budesonide.

Early treatment of chlorine-induced airway hyperresponsiveness and inflammation with corticosteroids.

Inflammation and airway hyperresponsiveness after chlorine exposure are prolonged by Nrf2 deficiency in mice.

Acute chlorine gas exposure produces transient inflammation and a progressive alteration in surfactant composition with accompanying mechanical dysfunction.

Abnormal epithelial structure and chronic lung inflammation after repair of chlorine-induced airway injury.

Chlorination of pyridinium compounds. Possible role of hypochlorite, N-chloramines, and chlorine in the oxidation of pyridinoline cross-links of articular cartilage collagen type II during acute inflammation.

[New chlorine derivatives of indole-3-acetic acid and their effect on experiments inflammation. I].

La base de données d'herbes médicinales la plus complète soutenue par la science

Anti-inflammatory drugs degradation during LED-UV ₃₆₅ photolysis of free chlorine: roles of reactive oxidative species and formation of disinfection by-products