ArticlePloS one2012
Alveolar macrophages play a key role in cockroach-induced allergic inflammation via TNF-α pathway.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Three Main SCFAs Mitigate Lung Inflammation and Tissue Remodeling Nlrp3-Dependent in Murine HDM-Induced Neutrophilic Asthma.Inflammation · 2024Article
- Airborne indoor allergen serine proteases and their contribution to sensitisation and activation of innate immunity in allergic airway disease.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Macrophages Orchestrate Airway Inflammation, Remodeling, and Resolution in Asthma.International journal of molecular sciences · 2023Review
- The influence ofFrontiers in pharmacology · 2023Article
- Herbal medicine for the treatment of obesity-associated asthma: a comprehensive review.Frontiers in pharmacology · 2023Review
- Cdc42 regulates cytokine expression and trafficking in bronchial epithelial cells.Frontiers in immunology · 2022Article
- Review
- The Role of T Cells and Macrophages in Asthma Pathogenesis: A New Perspective on Mutual Crosstalk.Mediators of inflammation · 2020Article
- GM-CSF produced by the airway epithelium is required for sensitization to cockroach allergen.Mucosal immunology · 2017Article
- In Utero exposure to genistein enhanced intranasal house dust mite allergen-induced respiratory sensitization in young adult B6C3F1 mice.Toxicology letters · 2016Article
- Morin Attenuates Ovalbumin-Induced Airway Inflammation by Modulating Oxidative Stress-Responsive MAPK Signaling.Oxidative medicine and cellular longevity · 2016Article
- Ganoderic acid C1 isolated from the anti-asthma formula, ASHMI™ suppresses TNF-α production by mouse macrophages and peripheral blood mononuclear cells from asthma patients.International immunopharmacology · 2015Article
- Renal F4/80+ CD11c+ mononuclear phagocytes display phenotypic and functional characteristics of macrophages in health and in adriamycin nephropathy.Journal of the American Society of Nephrology : JASN · 2015Article
- Obesity increases airway hyperresponsiveness via the TNF-α pathway and treating obesity induces recovery.PloS one · 2015Article
- Current status of standardization of inhalant allergen extracts in Korea.Allergy, asthma & immunology research · 2014Review
- Dysregulation of alveolar macrophages unleashes dendritic cell-mediated mechanisms of allergic airway inflammation.Mucosal immunology · 2014Article
- The effects of maekmoondong-tang on cockroach extract-induced allergic asthma.Evidence-based complementary and alternative medicine : eCAM · 2014Article
- Evaluation on potential contributions of protease activated receptors related mediators in allergic inflammation.Mediators of inflammation · 2014Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activity of the serine protease in the German cockroach allergen is important to the development of allergic disease. The protease-activated receptor (PAR)-2, which is expressed in numerous cell types in lung tissue, is known to mediate the cellular events caused by inhaled serine protease. Alveolar macrophages express PAR-2 and produce considerable amounts of tumor necrosis factor (TNF)-α. We determined whether the serine protease in German cockroach extract (GCE) enhances TNF-α production by alveolar macrophages through the PAR-2 pathway and whether the TNF-α production affects GCE-induced pulmonary inflammation. Effects of GCE on alveolar macrophages and TNF-α production were evaluated using in vitro MH-S and RAW264.6 cells and in vivo GCE-induced asthma models of BALB/c mice. GCE contained a large amount of serine protease. In the MH-S and RAW264.7 cells, GCE activated PAR-2 and thereby produced TNF-α. In the GCE-induced asthma model, intranasal administration of GCE increased airway hyperresponsiveness (AHR), inflammatory cell infiltration, productions of serum immunoglobulin E, interleukin (IL)-5, IL-13 and TNF-α production in alveolar macrophages. Blockade of serine proteases prevented the development of GCE induced allergic pathologies. TNF-α blockade also prevented the development of such asthma-like lesions. Depletion of alveolar macrophages reduced AHR and intracellular TNF-α level in pulmonary cell populations in the GCE-induced asthma model. These results suggest that serine protease from GCE affects asthma through an alveolar macrophage and TNF-α dependent manner, reflecting the close relation of innate and adaptive immune response in allergic asthma model.
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