ArticleBritish journal of pharmacology2003
Involvement of tachykinin receptors in Clostridium perfringens beta-toxin-induced plasma extravasation.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Blood proteome profiling for biomarker discovery in broilers with necrotic enteritis.Scientific reports · 2025Article
- METTL3 Regulates the Inflammatory Response in CPB2 Toxin-Exposed IPEC-J2 Cells through the TLR2/NF-κB Signaling Pathway.International journal of molecular sciences · 2022Article
- Molecular docking analysis of P2X7 receptor with the beta toxin from Clostridium perfringens.Bioinformation · 2020Article
- Review
- Mechanisms of Action and Cell Death Associated withToxins · 2018Review
- Molecular Evolutionary Constraints that Determine the Avirulence State of Clostridium botulinum C2 Toxin.Journal of molecular evolution · 2017Article
- Animal models to study the pathogenesis of human and animal Clostridium perfringens infections.Veterinary microbiology · 2015Review
- Review
- Review
- The p38 MAPK and JNK pathways protect host cells against Clostridium perfringens beta-toxin.Infection and immunity · 2013Article
- Role of pore-forming toxins in bacterial infectious diseases.Microbiology and molecular biology reviews : MMBR · 2013Review
- Recent progress in understanding the pathogenesis of Clostridium perfringens type C infections.Veterinary microbiology · 2011Review
- Article
- Involvement of tumour necrosis factor-alpha in Clostridium perfringens beta-toxin-induced plasma extravasation in mice.British journal of pharmacology · 2008Article
- Cloning of alpha-beta fusion gene from Clostridium perfringens and its expression.World journal of gastroenterology · 2006Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1 Clostridium perfringens beta-toxin causes dermonecrosis and oedema in the dorsal skin of animals. In the present study, we investigated the mechanisms of oedema induced by the toxin. 2 The toxin induced plasma extravasation in the dorsal skin of Balb/c mice. 3 The extravasation was significantly inhibited by diphenhydramine, a histamine 1 receptor antagonist. However, the toxin did not cause the release of histamine from mouse mastocytoma cells. 4 Tachykinin NK(1) receptor antagonists, [D-Pro(2), D-Trp(7,9)]-SP, [D-Pro(4), D-Trp(7,9)]-SP and spantide, inhibited the toxin-induced leakage in a dose-dependent manner. Furthermore, the non-peptide tachykinin NK(1) receptor antagonist, SR140333, markedly inhibited the toxin-induced leakage. 5 The leakage induced by the toxin was markedly reduced in capsaicin-pretreated mouse skin but the leakage was not affected by systemic pretreatment with a calcitonin gene-related peptide receptor antagonist (CGRP(8-37)). 6 The toxin-induced leakage was significantly inhibited by the N-type Ca(2+) channel blocker, omega-conotoxin MVIIA, and the bradykinin B(2) receptor antagonist, HOE140 (D-Arg-[Hyp(3), Thi(5), D-Tic(7), Oic(8)]-bradykinin), but was not affected by the selective L-type Ca(2+) channel blocker, verapamil, the P-type Ca(2+) channel blocker, omega-agatoxin IVA, tetrodotoxin (TTX), the TTX-resistant Na(+) channel blocker, carbamazepine, or the sensory nerve conduction blocker, lignocaine. 7 These results suggest that plasma extravasation induced by beta-toxin in mouse skin is mediated via a mechanism involving tachykinin NK(1) receptors.
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