Oral Administration of Acrylamide Worsens the Inflammatory Responses in the Airways of Asthmatic Mice Through Agitation of Oxidative Stress in the Lungs

Hajimohammadi, Bahador; Athari, Seyyede Masoume; Abdollahi, Mohammad; Vahedi, Ghasem; Athari, Seyyed Shamsadin

doi:10.3389/fimmu.2020.01940

Cited by 24 publications

(16 citation statements)

References 38 publications

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“…Oxidative stress is a crucial factor in the pathophysiology of allergic asthma. Previous studies have provided a potential link between increased oxidative damage and the development, or worsening of allergic asthma [ 32 ]. In this study, exacerbated allergic asthma symptoms were found in the atopic march group compared with the OVA group, accompanied by the induction of pulmonary tissue oxidative stress, as indicated by decreased GSH and increased MDA levels ( Figure 7 A,B).…”

Section: Discussionmentioning

confidence: 99%

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

Li¹,

Zhang²,

Ren

et al. 2021

Bioscience Reports

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Purpose: The pathological process of atopic dermatitis (AD) progressing into other types of allergic diseases such as asthma and allergic rhinitis during the first several years of life is often referred to as the atopic march. Although the phenomenon of atopic march has been recognized for decades, how asthma stems from AD is still not fully understood, confounding a universal strategy to effectively protect people from the atopic march. Methods: We established experimental atopic march mice by first inducing allergic dermatitis with 0.5% fluorescein isothiocyante applied to the skin, followed by an OVA airway challenge. In addition, by examining serum immunoglobulin concentrations, airway cytokines, the levels of oxidative stress markers, histopathological changes in lung tissue and airway hyperresponsiveness, we were able to validate the successful establishment of the model. Furthermore, by detecting the attenuating effects of melatonin (MT) and the levels of oxidative stress in the atopic march mice, we explored the potential molecular mechanisms involved in the development of atopic march. Results: By successfully establishing an experimental atopic march mouse model, we were able to demonstrate that overproduction of oxidative stress in the lung significantly upregulated the activation of NF-κB signaling pathways causing TSLP release, which further promotes the development of atopic march. Conclusions: To mitigate the development of the atopic march, antioxidants such as MT may be imperative to inhibit NF-κB activation in the lung, especially after the onset of AD.

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Section: Discussionmentioning

confidence: 99%

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

Li¹,

Zhang²,

Ren

et al. 2021

Bioscience Reports

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“…Interleukin (IL)-4, IL-5, IL-9 and IL-13 are important cytokines that play key roles in type 2 immunity, and are usually involved in allergic diseases or during helminthic parasitic infections (8,9). Th2 cells and certain myeloid cells are considered the primary source of these type 2 cytokines (10,11); however, recent studies have reported that a rare subpopulation of innate lymphocytes are the predominant source (12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

A crosstalk between type 2 innate lymphoid cells and alternative macrophages in lung development and lung diseases (Review)

Zhu

Lü

2021

Mol Med Rep

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Type 2 innate lymphoid cells (ILC2s) are important innate immune cells that are involved in type 2 inflammation, in both mice and humans. ILC2s are stimulated by factors, including interleukin (IL)-33 and IL-25, and activated ILC2s secrete several cytokines that mediate type 2 immunity by inducing profound changes in physiology, including activation of alternative (M2) macrophages. M2 macrophages possess immune modulatory, phagocytic, tissue repair and remodeling properties, and can regulate ILC2s under infection. The present review summarizes the role of ILC2s as innate cells and M2 macrophages as anti-inflammatory cells, and discusses current literature on their important biological significance. The present review also highlights how the crosstalk between ILC2s and M2 macrophages contributes to lung development, induces pulmonary parasitic expulsion, exacerbates pulmonary viral and fungal infections and allergic airway diseases, and promotes the development of lung diseases, such as pulmonary fibrosis, chronic obstructive pulmonary disease and carcinoma of the lungs. Contents

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“…For example, a comparatively increased airway resistance at a lower versus higher MCh concentration would indicate a hyper-reactive airway response. The maximum tested MCh concentration was limited to 0.5 mg/mL because OVA-exposed mice exhibited severe dyspnea and could not tolerate higher concentrations found in preliminary studies [ 38 , 39 ].…”

Section: Methodsmentioning

confidence: 99%

Novel aerosol treatment of airway hyper-reactivity and inflammation in a murine model of asthma with a soluble epoxide hydrolase inhibitor

Zhang

et al. 2022

PLoS ONE

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Asthma currently affects more than 339 million people worldwide. In the present preliminary study, we examined the efficacy of a new, inhalable soluble epoxide hydrolase inhibitor (sEHI), 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), to attenuate airway inflammation, mucin secretion, and hyper-responsiveness (AHR) in an ovalbumin (OVA)-sensitized murine model. Male BALB/c mice were divided into phosphate-buffered saline (PBS), OVA, and OVA+TPPU (2- or 6-h) exposure groups. On days 0 and 14, the mice were administered PBS or sensitized to OVA in PBS. From days 26–38, seven challenge exposures were performed with 30 min inhalation of filtered air or OVA alone. In the OVA+TPPU groups, a 2- or 6-h TPPU inhalation preceded each 30-min OVA exposure. On day 39, pulmonary function tests (PFTs) were performed, and biological samples were collected. Lung tissues were used to semi-quantitatively evaluate the severity of inflammation and airway constriction and the volume of stored intracellular mucosubstances. Bronchoalveolar lavage (BAL) and blood samples were used to analyze regulatory lipid mediator profiles. Significantly (p < 0.05) attenuated alveolar, bronchiolar, and pleural inflammation; airway resistance and constriction; mucosubstance volume; and inflammatory lipid mediator levels were observed with OVA+TPPU relative to OVA alone. Cumulative findings indicated TPPU inhalation effectively inhibited inflammation, suppressed AHR, and prevented mucosubstance accumulation in the murine asthmatic model. Future studies should determine the pharmacokinetics (i.e., absorption, distribution, metabolism, and excretion) and pharmacodynamics (i.e., concentration/dose responses) of inhaled TPPU to explore its potential as an asthma-preventative or -rescue treatment.

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Oral Administration of Acrylamide Worsens the Inflammatory Responses in the Airways of Asthmatic Mice Through Agitation of Oxidative Stress in the Lungs

Cited by 24 publications

References 38 publications

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

A crosstalk between type 2 innate lymphoid cells and alternative macrophages in lung development and lung diseases (Review)

Novel aerosol treatment of airway hyper-reactivity and inflammation in a murine model of asthma with a soluble epoxide hydrolase inhibitor

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