ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
TRPA1 controls inflammation and pruritogen responses in allergic contact dermatitis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
118 citing papers in PubMed, 222 citations in OpenAlex.
- Review
- The Mast Cell-Substance P Neuroimmune Axis in Allergic Contact Dermatitis and Atopic Dermatitis: Molecular Mechanisms and Pathophysiological Perspectives.Current issues in molecular biology · 2026Review
- Mechanisms of pruritus and advances in traditional Chinese medicine therapy (Review).Molecular medicine reports · 2026Review
- From neuroimmune circuits to targeted therapy of chronic pruritus.Pharmacological reviews · 2026Review
- Article
- Pathophysiologic Mechanisms and Targeted Treatments Associated with the Nervous System in Cutaneous Allergic Diseases.Clinical reviews in allergy & immunology · 2025Review
- Allergic Contact Dermatitis: Immunopathology and Potential Therapeutic Strategies.Journal of clinical medicine · 2025Review
- The Contact Allergen Methylisothiazolinone (MIT) is a Potent Activator of the TRPA1 Ion Channel.Pharmacology research & perspectives · 2025Article
- Molecular and cellular mechanisms of itch sensation and the anti-itch drug targets.Acta pharmacologica Sinica · 2025Review
- Wenqing Yin Attenuates the Allergic Contact Dermatitis Response by Inhibiting the JAK2/STAT1 and MAPK Signaling Pathways.Journal of inflammation research · 2025Article
- Pharmacologic Inhibition of Transient Receptor Potential Ion Channel Ankyrin 1 Counteracts 2-Chlorobenzalmalononitrile Tear Gas Agent-Induced Cutaneous Injuries.The Journal of pharmacology and experimental therapeutics · 2024Article
- Site-Specific Transient Receptor Potential Channel Mechanisms and Their Characteristics for Targeted Chronic Itch Treatment.Biomolecules · 2024Review
- Targeting Transient Receptor Potential (TRP) Channels, Mas-Related G-Protein-Coupled Receptors (Mrgprs), and Protease-Activated Receptors (PARs) to Relieve Itch.Pharmaceuticals (Basel, Switzerland) · 2023Review
- An update on mechanisms of pruritus and their potential treatment in primary cutaneous T-cell lymphoma.Clinical and experimental medicine · 2023Review
- A Novel Flp Reporter Mouse Shows That TRPA1 Expression Is Largely Limited to Sensory Neuron Subsets.eNeuro · 2023Article
- Pathomechanism of Pruritus in Psoriasis and Atopic Dermatitis: Novel Approaches, Similarities and Differences.International journal of molecular sciences · 2023Review
- Molecular Mechanisms of Neurogenic Inflammation of the Skin.International journal of molecular sciences · 2023Review
- Inflammation-the role of TRPA1 channel.Frontiers in physiology · 2023Review
- CYP1B1-derived epoxides modulate the TRPA1 channel in chronic pain.Acta pharmaceutica Sinica. B · 2023Article
- Transient Receptor Potential Channels and Itch.International journal of molecular sciences · 2022Review
58 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Allergic contact dermatitis is a common skin disease associated with inflammation and persistent pruritus. Transient receptor potential (TRP) ion channels in skin-innervating sensory neurons mediate acute inflammatory and pruritic responses following exogenous stimulation and may contribute to allergic responses. Genetic ablation or pharmacological inhibition of TRPA1, but not TRPV1, inhibited skin edema, keratinocyte hyperplasia, nerve growth, leukocyte infiltration, and antihistamine-resistant scratching behavior in mice exposed to the haptens, oxazolone and urushiol, the contact allergen of poison ivy. Hapten-challenged skin of TRPA1-deficient mice contained diminished levels of inflammatory cytokines, nerve growth factor, and endogenous pruritogens, such as substance P (SP) and serotonin. TRPA1-deficient sensory neurons were defective in SP signaling, and SP-induced scratching behavior was abolished in Trpa1(-/-) mice. SP receptor antagonists, such as aprepitant inhibited both hapten-induced cutaneous inflammation and scratching behavior. These findings support a central role for TRPA1 and SP in the integration of immune and neuronal mechanisms leading to chronic inflammatory responses and pruritus associated with contact dermatitis.
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Registered trials
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.