Cutaneous responses to vasoactive intestinal polypeptide in chronic idiopathic urticaria

Smith, Catherine; Atkinson, Beryl A.; Morris, Richard W; Hayes, N.A.; Foreman, J. C.; Lee, T H

doi:10.1016/0140-6736(92)91000-x

Cited by 38 publications

(16 citation statements)

References 10 publications

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“…Smith et al . reported a significant increase in VIP‐induced weal in urticarial plaques and increased sensitivity of microvasculature to VIP in patients with CU.…”

Section: Discussionmentioning

confidence: 99%

Effects of loratadine and cetirizine on serum levels of neuropeptides in patients with chronic urticaria

et al. 2014

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H1-receptor inhibiting drugs, namely loratadine and cetirizine, were frequently used in treatment of chronic urticaria. Urticarial weal and flare reactions, a neurogenic reflex due to neuropeptides, were reported to be more effectively inhibited by cetirizine than loratadine. The aim of this study was to determine and compare the effects of systemic loratadine and cetirizine treatments on serum levels of selected neuropeptides in chronic urticaria. Treatment groups of either systemic loratadine or cetirizine (10 mg/d), consisting of 16 and 22 patients, respectively, were included. Serum levels of stem cell factor (SCF), neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), nerve growth factor (NGF), vasoactive intestinal peptide (VIP), and substance P (SP) were detected before and after one week of treatment with antihistamines. Serum NPY and VIP levels were significantly decreased when compared before and after treatment with antihistamines (P < 0.001 and P < 0.01, respectively). SCF and NGF values were also decreased after antihistamine treatment (P < 0.05). Post-treatment levels of CGRP were significantly higher compared with pretreatment values, while no significant difference was detected between pre and post treatment levels of SP. Cetirizine was significantly more effective than loratadine on lowering serum levels of SCF among the other neuropeptides. Systemic loratadine and cetirizine treatments in patients with chronic urticaria precisely caused variations in serum levels of neuropeptides. The predominant effect of cetirizine compared to loratadine on reducing serum SCF levels might be explained with anti-inflammatory properties of cetirizine.

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“…Smith et al . reported a significant increase in VIP‐induced weal in urticarial plaques and increased sensitivity of microvasculature to VIP in patients with CU.…”

Section: Discussionmentioning

confidence: 99%

Effects of loratadine and cetirizine on serum levels of neuropeptides in patients with chronic urticaria

et al. 2014

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“…Initial studies indicated increased activity of compound 48/80 in non‐lesional skin of CSU patients, which became normal in remission . The skin of CSU patients has also been reported to show increased responsiveness to the neuropeptides substance P and VIP . One mechanism of this enhanced reactivity has been shown recently to be a significantly higher expression of MrgX2, the receptor for compound 48/80 and neuropeptides, on skin mast cells from CSU patients compared with those from healthy individuals .…”

Section: Is Mast Cell Reactivity Changed?mentioning

confidence: 99%

The role and relevance of mast cells in urticaria

Church

Kolkhir

Metz

et al. 2018

Immunological Reviews

208

198

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This review presents evidence that the skin mast cell, in particular the MC subtype, is the primary effector cell in urticaria. Mast cells are located in the upper dermis, the ideal situation for wheal formation and sensory nerve stimulation. Increased numbers of mast cells are found in both lesional and non-lesional skin in CSU and inducible urticaria. Mast cell degranulation in the area of wheals has been demonstrated repeatedly by light and electron microscopy. Histamine, PGD and tryptase are found in the venous blood draining wheal formation. The last 2 are specific for mast cells rather than basophils. Mast cell reactivity is increased in active urticaria by local inflammatory cytokines and neuropeptides. Mast cell cytokines and neuropeptides, particularly nerve growth factor, induce a Th2 type inflammation that is particularly obvious at the sites of whealing. In conclusion, autoimmunity, either of Type 1 viz. IgE antibodies to local autoallergens, or Type 2b, viz. IgG autoantibodies to IgE or its receptor, are considered to be the most frequent causes of CSU. In both cases, the mast cell is likely to be the axial cell in producing the wheals.

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“…Pre-treatment with RR at LI11 altered the antipruritic effects of 20°C thermal stimulation at LI11, suggesting that peripheral TRP ion channels may play a role in this effect. Since compound 48/80, a basic polypeptide with potent mast cell degranulating ability, can induce the flare and weal responses after intradermal injected, this pruritogenic agent is conducted in the study of inducing urticaria and the pruritus of atopic dermatitis [41–43]. …”

Section: Discussionmentioning

confidence: 99%

Antipruritic effect of cold stimulation at the Quchi Acupoint (LI11) in Mice

Tsai

Chen

et al. 2014

BMC Complement Altern Med

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BackgroundAcupuncture and moxibustion are used to treat pruritus and atopic dermatitis. However, whether cold stimulation (defined as that the temperature conducted under skin temperature) of acupoints affects itching in experimental murine models remains unclear.MethodsThe present study was designed to determine the therapeutic effects of different thermal stimulations at the Quchi acupoint (LI11) in a murine model in which scratching behaviour was elicited by subcutaneous injection with a pruritogenic agent (compound 48/80). Male ICR mice were divided into several groups as follows: control (saline), those receiving compound 48/80 and compound 48/80 with various thermal stimulations (5°C–45°C) at LI11 (n = 6 per group). The scratch response of each animal to these stimulations was recorded for 30 min. The antipruritic effect of the acupoint was further evaluated in LI11 and sham (non-acupoint) groups (n = 6 per group).ResultsTreatment with lower temperature (20°C) at the LI11 acupoint significantly attenuated compound 48/80-induced scratching; however, this antipruritic effect was not observed with stimulation at the sham point. The expression of c-fos in the neuron of the cervical spine induced by compound 48/80 was suppressed by cold stimulation at LI11. The antipruritic effect of cold stimulation was blocked by ruthium red (RR), a non-selective transient receptor potential (TRP) channel blocker, suggesting that TRP channels may play an important role in the antipruritic effect of cold stimulation at LI11 in mice.ConclusionsThis study demonstrated that cold stimulation at LI11 attenuated compound 48/80-induced scratching behaviour in mice, possibly by a TRP-related pathway.

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Cutaneous responses to vasoactive intestinal polypeptide in chronic idiopathic urticaria

Cited by 38 publications

References 10 publications

Effects of loratadine and cetirizine on serum levels of neuropeptides in patients with chronic urticaria

Effects of loratadine and cetirizine on serum levels of neuropeptides in patients with chronic urticaria

The role and relevance of mast cells in urticaria

Antipruritic effect of cold stimulation at the Quchi Acupoint (LI11) in Mice

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