ArticleBritish journal of pharmacology2008
Evidence for the role of neurogenic inflammation components in trypsin-elicited scratching behaviour in mice.
Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 89 citations in OpenAlex.
- Trial
- Prevalence and Mechanisms of Itch in Chronic Wounds: A Narrative Review.Journal of clinical medicine · 2025Review
- The Effect of Osthole on Transient Receptor Potential Channels: A Possible Alternative Therapy for Atopic Dermatitis.Journal of inflammation research · 2024Article
- Molecular mechanisms of pruritus in prurigo nodularis.Frontiers in immunology · 2023Review
- Generalized resistance to pruritogen-induced scratching in the C3H/HeJ strain.Frontiers in molecular neuroscience · 2022Article
- Intractable Itch in Atopic Dermatitis: Causes and Treatments.Biomedicines · 2021Review
- Desensitization of TRPV1 Involved in the Antipruritic Effect of Osthole on Histamine-Induced Scratching Behavior in Mice.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- The TRPM3 ion channel mediates nociception but not itch evoked by endogenous pruritogenic mediators.Biochemical pharmacology · 2021Article
- IL-31 and IL-8 in Cutaneous T-Cell Lymphoma: Looking for Their Role in Itch.Advances in hematology · 2021Article
- Riboflavin Inhibits Histamine-Dependent Itch by Modulating Transient Receptor Potential Vanilloid 1 (TRPV1).Frontiers in molecular neuroscience · 2021Article
- Cholestasis-Associated Pruritus and Its Pruritogens.Frontiers in medicine · 2021Review
- Amelioration of Compound 48/80-Mediated Itch and LL-37-Induced Inflammation by a Single-Stranded Oligonucleotide.Frontiers in immunology · 2020Article
- TRP Channels as Drug Targets to Relieve Itch.Pharmaceuticals (Basel, Switzerland) · 2018Review
- A Nonsteroidal Novel Formulation Targeting Inflammatory and Pruritus-Related Mediators Modulates Experimental Allergic Contact Dermatitis.Dermatology and therapy · 2018Article
- Sildenafil Treatment Eliminates Pruritogenesis and Thermal Hyperalgesia in Rats with Portacaval Shunts.Neurochemical research · 2017Article
- Mediators of Chronic Pruritus in Atopic Dermatitis: Getting the Itch Out?Clinical reviews in allergy & immunology · 2016Review
- Osthole inhibits histamine-dependent itch via modulating TRPV1 activity.Scientific reports · 2016Article
- Hydrogen sulfide-induced itch requires activation of Cav3.2 T-type calcium channel in mice.Scientific reports · 2015Article
- Mechanisms Underlying the Scratching Behavior Induced by the Activation of Proteinase-Activated Receptor-4 in Mice.The Journal of investigative dermatology · 2015Article
- Protease-activated receptors and itch.Handbook of experimental pharmacology · 2015Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeWe investigated the mechanisms underlying the pruritogenic response induced by trypsin in mice, to assess the relevance of neurogenic inflammation components in this response. EXPERIMENTAL APPROACH: Itching was induced by an intradermal injection of trypsin in the mouse neck. The animals were observed for 40 min and their scratching behaviour was quantified. KEY
resultsTrypsin-induced itching was blocked by the lima bean trypsin inhibitor, the selective proteinase-activated receptor-2 (PAR-2) antagonist FSLLRY and PAR-2 receptor desensitization. An important involvement of mast cells was observed, as chronic pretreatment with the mast cell degranulator compound 48/80 or the mast cell stabilizer disodium cromoglycate prevented scratching. Also, trypsin response was inhibited by the selective COX-2 inhibitor celecoxib and by the selective kinin B2 (FR173657) and B1 (SSR240612) receptor antagonists. Moreover, an essential role for the mediators of neurogenic inflammation was established, as the selective NK1 (FK888), NK3 (SR142801) and calcitonin gene-related peptide (CGRP(8-37) fragment) receptor antagonists inhibited trypsin-induced itching. Similarly, blockade of transient receptor potential vanilloid 1 (TRPV1) receptors by the selective TRPV1 receptor antagonist SB366791, or by genetic deletion of TRPV1 receptor reduced this behaviour in mice. C-fibre desensitization showed a very similar result. CONCLUSIONS AND IMPLICATIONS: Trypsin intradermal injection proved to be a reproducible model for the study of itching and the involvement of PAR-2 receptors. Also, trypsin-induced itching seems to be widely dependent on neurogenic inflammation, with a role for TRPV1 receptors. In addition, several other mediators located in the sensory nerves and skin also seem to contribute to this process.
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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.