Melatonin antagonizes ozone-exacerbated asthma by inhibiting the TRPV1 channel and stabilizing the Nrf2 pathway

Chen, Yu‐Shan; Wu, Xiaoyu; Xu, Yujie; Li, Xudong; Zeng, Yan; Li, Jinquan

doi:10.1007/s11356-021-14945-9

Cited by 12 publications

(12 citation statements)

References 52 publications

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“…These results suggest that in comparison to the OVA-induced mice, the experimental atopic march model mice demonstrated an exacerbated inflammation response. In addition, the added effects of AD on OVA-induced allergic asthma were also confirmed by lung histopathological changes and AHR [31]. More serious airway remolding, worsened inflammatory cell infiltration, increased mucus secretion, and increased AHR, were all observed in the atopic march mice (Fig 4 and 5).…”

Section: Discussionmentioning

confidence: 65%

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: 65%

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

Li¹,

Zhang²,

Ren

et al. 2021

Bioscience Reports

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“…They do so by detecting environmental danger, triggering an avoidance response, and by tuning immune responses. In the context of allergy, nociceptor neurons were found to amplify dermatitis (10, 15, 16, 45), conjunctivitis (46) and airway inflammation (14, 22, 27, 28, 47, 48). In the lungs, these responses range from coughing and bronchoconstriction to mucus secretion and, depending on the context, amplifying, or taming immunity.…”

Section: Discussionmentioning

confidence: 99%

Cytokines reprogram airway sensory neurons in asthma

Crosson

Bhat

Wang

et al. 2023

Preprint

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Nociceptor neurons play a crucial role in maintaining the body's equilibrium by detecting and responding to potential dangers in the environment. However, this function can be detrimental during allergic reactions, since vagal nociceptors can contribute to immune cell infiltration, bronchial hypersensitivity, and mucus imbalance, in addition to causing pain and coughing. Despite this, the specific mechanisms by which nociceptors acquire pro-inflammatory characteristics during allergic reactions are not yet fully understood. In this study, we aimed to investigate the molecular profile of airway nociceptor neurons during allergic airway inflammation and identify the signals driving such reprogramming. Using retrograde tracing and lineage reporting, we identified a class of inflammatory vagal nociceptor neurons that exclusively innervate the airways. Using an ovalbumin mouse model of airway inflammation, we found that these neurons undergo significant reprogramming characterized by the upregulation of the NPY receptor Npy1r, along with Il6. A screening of asthma-driving cytokines revealed that IL-13 drives part of this reprogramming, including Npy1r overexpression via the JAK/STAT6 pathway, while IL-1β induces IL-6 expression and release. Additionally, we observed that sympathetic neurons release NPY in the bronchoalveolar fluid of asthmatic mice, which limits the excitability of nociceptor neurons. In summary, allergic airway inflammation reprograms airway nociceptor neurons to acquire a pro-inflammatory phenotype, characterized by the release of IL-6, while a compensatory mechanism involving NPY1R limits nociceptor neurons' activity.

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“…These studies have suggested that melatonin suppresses IgE production by inhibiting the IL‐4/STAT6 pathway and promoting IL‐21/STAT3 pathway. In vivo studies have demonstrated that melatonin decreases serum IgE levels and antigen‐specific IgE level 41,120 . Melatonin also induces NFIL3 expression, 121–123 which might promote IgE transcription 124 .…”

Section: Melatonin Modulates Food Allergy Through the Immune System: ...mentioning

confidence: 99%

Melatonin in food allergy: Mechanism and potential therapy

Wang

Yan

Hung³

et al. 2023

Journal of Pineal Research

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Food allergy affects more than 500 million people in the world, and its prevalence is increasing at an alarming rate causing serious public health concerns; however, prevention and treatment methods are still under investigation and are relatively scarce so far. Insights on pathophysiology reveal a complex interplay of the immune cells (e.g., DCs, T cells, and B cells) resulting in allergy or tolerance. Studies have shown that melatonin metabolisms are altered in patients with allergic diseases, suggesting that melatonin might impact allergic diseases. Notably, melatonin can orchestrate the differentiation and function of immune cells. Additionally, the disease severities of many allergic diseases and the function of the immune system exhibit circadian rhythmicity. Therefore, melatonin, a rhythm regulator, may also act indirectly on the immune system through the circadian clock to regulate food allergies. Herein, we reviewed the impacts of melatonin on food allergy and its underlying regulatory mechanisms, providing a theoretical reference for melatonin as effective means of prevention and treatment for food allergy in the future.

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Melatonin antagonizes ozone-exacerbated asthma by inhibiting the TRPV1 channel and stabilizing the Nrf2 pathway

Cited by 12 publications

References 52 publications

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

Cytokines reprogram airway sensory neurons in asthma

Melatonin in food allergy: Mechanism and potential therapy

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