ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Inhaled birch pollen extract induces airway hyperresponsiveness via oxidative stress but independently of pollen-intrinsic NADPH oxidase activity, or the TLR4-TRIF pathway.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
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- ATP functions as a primary alarmin in allergen-induced type 2 immunity.American journal of physiology. Cell physiology · 2023Review
- Distinction between rhinitis alone and rhinitis with asthma using interactomics.Scientific reports · 2023Article
- Oxidative Stress and Antioxidants in Chronic Rhinosinusitis with Nasal Polyps.Antioxidants (Basel, Switzerland) · 2023Review
- When the allergy alarm bells toll: The role of Toll-like receptors in allergic diseases and treatment.Frontiers in molecular biosciences · 2023Review
- How Do Pollen Allergens Sensitize?Frontiers in molecular biosciences · 2022Review
- Role of Nrf2 in Disease: Novel Molecular Mechanisms and Therapeutic Approaches - Pulmonary Disease/Asthma.Frontiers in physiology · 2021Review
- Birch Pollen Induces Toll-Like Receptor 4-Dependent Dendritic Cell Activation Favoring T Cell Responses.Frontiers in allergy · 2021Article
- Interactive Roles of CaMKII/Ryanodine Receptor Signaling and Inflammation in Lung Diseases.Advances in experimental medicine and biology · 2021Review
- Asthma: New Integrative Treatment Strategies for the Next Decades.Medicina (Kaunas, Lithuania) · 2020Review
- Effect ofPostepy dermatologii i alergologii · 2020Article
- Initiating pollen sensitization - complex source, complex mechanisms.Clinical and translational allergy · 2020Review
- Generation of Superoxide by OeRbohH, a NADPH Oxidase Activity During Olive (Frontiers in plant science · 2019Article
- miR-155 Modulates Cockroach Allergen- and Oxidative Stress-Induced Cyclooxygenase-2 in Asthma.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Probiotics against airway allergy: host factors to consider.Disease models & mechanisms · 2018Review
- The TLR4-TRIF pathway can protect against the development of experimental allergic asthma.Immunology · 2017Article
- Cationic CaMKII Inhibiting Nanoparticles Prevent Allergic Asthma.Molecular pharmaceutics · 2017Article
- Oxidized CaMKII promotes asthma through the activation of mast cells.JCI insight · 2017Article
- Proteases and oxidant stress control organic dust induction of inflammatory gene expression in lung epithelial cells.Respiratory research · 2016Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Oxidative stress in allergic asthma may result from oxidase activity or proinflammatory molecules in pollens. Signaling via TLR4 and its adaptor Toll-IL-1R domain-containing adapter inducing IFN-β (TRIF) has been implicated in reactive oxygen species-mediated acute lung injury and in Th2 immune responses. We investigated the contributions of oxidative stress and TLR4/TRIF signaling to experimental asthma induced by birch pollen exposure exclusively via the airways. Mice were exposed to native or heat-inactivated white birch pollen extract (BPEx) intratracheally and injected with the antioxidants, N-acetyl-L-cysteine or dimethylthiourea, prior to sensitization, challenge, or all allergen exposures, to assess the role of oxidative stress and pollen-intrinsic NADPH oxidase activity in allergic sensitization, inflammation, and airway hyperresponsiveness (AHR). Additionally, TLR4 signaling was antagonized concomitantly with allergen exposure, or the development of allergic airway disease was evaluated in TLR4 or TRIF knockout mice. N-acetyl-L-cysteine inhibited BPEx-induced eosinophilic airway inflammation and AHR except when given exclusively during sensitization, whereas dimethylthiourea was inhibitory even when administered with the sensitization alone. Heat inactivation of BPEx had no effect on the development of allergic airway disease. Oxidative stress-mediated AHR was also TLR4 and TRIF independent; however, TLR4 deficiency decreased, whereas TRIF deficiency increased BPEx-induced airway inflammation. In conclusion, oxidative stress plays a significant role in allergic sensitization to pollen via the airway mucosa, but the pollen-intrinsic NADPH oxidase activity and TLR4 or TRIF signaling are unnecessary for the induction of allergic airway disease and AHR. Pollen extract does, however, activate TLR4, thereby enhancing airway inflammation, which is restrained by the TRIF-dependent pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.