Possible roles of basophils in chronic itch

Abstract

Basophils are blood granulocytes and normally constitute <1% of blood peripheral leucocytes. Basophils share some morphological and functional similarities with mast cells, and basophils were once regarded as redundant and negligible circulating mast cells. However, recent studies reveal the indispensable roles of basophils in various diseases, including allergic and pruritic diseases. Basophils may be involved in itch through the mediation of a Th2 immune response, interaction with other cells in the skin and secretion of a wide variety of itch-related mediators, for example histamine, cytokines and chemokines (IL-4, IL-13, IL-31 and TSLP), proteases (cathepsin S), prostaglandins (PGE2 and PGD2), substance P and platelet-activating factor. Not only pruritic skin diseases (eg, atopic dermatitis, irritant contact dermatitis, chronic urticaria, prurigo, papulo-erythroderma of Ofuji, eosinophilic pustular folliculitis, scabies, tick bites and bullous pemphigoid) but also pruritic systemic diseases (eg, primary sclerosing cholangitis and polycythemia vera) may be affected by basophils.

Prurigo successfully treated with duloxetine hydrochloride

“…In addition, a number of dermal basophils were observed as detected by BB1 antibody, which was consistent with a prior report (Fig. d) . Direct immunofluorescence findings (DIF) were negative.…”

Interaction of peripheral nerves and mast cells, eosinophils, and basophils in the development of pruritus

“…Basophils also express pruritus‐related mediators such as histamine, substance P, NGF, Th2 cytokines (eg IL‐4, IL‐13, IL‐31 and thymic stromal lymphopoietin [TSLP]), PGD 2 and PGE 2 , and proteases (eg cathepsin S) . Basophils, with ability to express a plethora of pruritogens, appear to have the potential to induce pruritus …”

Adverse effects of platelet-rich plasma and microneedling

“…Transitory scalp pruritus can potentially be explained through the effect of interleukin (IL) 31, recently described as one of the main itch mediators. 3 Upon wounding, transient inflammation causes migration of mast cells into the injured tissue. Thus, secretion of a variety of itch-related mediators-histamine, cytokines and chemokines (IL-4, IL-13, IL-31, and thymic stromal lymphopoietin), proteases (cathepsin S), prostaglandins, substance P, and platelet-activating factor-may be implicated.…”

“…1 Obesity might have a role in disease initiation or exacerbation by way of mechanical friction within skin folds resulting in follicular hyperkeratinization, a humid skin milieu favoring microbial overgrowth, and a systemic inflammatory state. [2][3][4] Although the association between obesity and HS is well established among adults, this relationship is poorly characterized in the pediatric population.…”