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NEUTROPHIL POLYMORPHONUCLEARS, MEDIATORS AND THE PATHOGENESIS OF PSORIASIS

The role of the neutrophil polymorphonuclear leukocyte in the pathogenesis of the psoriatic lesion is the subject of sustained interest. The presence of neutrophils within the acanthotic epidermis is a familiar histological feature of psoriasis, but the relationship of neutrophils to the histogenesis of psoriasis has been actively debated. Pinkus & Mehregan (1966) proposed that neutrophils gained access to the epidermis through the intermittent action of a 'squirting papilla', increase in epidermal mitotic activity being a consequence of this process. Subsequent attempts to confirm the concept of neutrophil immigration into epidermis as the prime histological event in the pathogenesis of psoriasis have been bedevilled by imprecise definitions ofthe 'earliest' lesion of psoriasis. Ragaz & Ackerman (1979) in a review of 300 biopsy samples (twenty from barely visible pinhead-size macules devoid of scales) observed early exocytosis of lymphocytes and histiocytes. However, the apparently abrupt appearance of neutrophil spongiform pustules in later papular lesions is puzzling and unexplained. Jablonska's studies of 'pre-pinpoint papules' in developing Koebner reactions produced by sellotape stripping revealed exocytosis of neutrophils into the epidermis as the earliest cellular change (Jablonska et al., 1982). This method can be criticized on the grounds that a papule is not necessarily the earliest stage in evolution of a psoriatic lesion. A more dynamic approach is clearly needed—perhaps an adaptation ofthe skin chamber method of Dubertret, Lebreton & Touraine (1982) to allow its use in the evolving psoriatic lesion. Notwithstanding these issues, neutrophil invasion of epidermis is a prominent event in psoriasis which serves to shift attention away from epidermal cell kinetics and growth control mechanisms and to strengthen mounting evidence of the importance of dermo-epidermal interaction in the genesis of psoriatic lesions. Because neutrophils are not only highly reactive to a wide range of autocoids, but are also themselves a Pandora's box of pharmacological activities, the molecular basis of neutrophil behaviour in psoriatic skin has begun to attract pharmacological attention. Examination of pharmacological reactivity of peripheral blood neutrophils to chemotactic and neutrophil-degranulating substances is an unsatisfactory approach and in practice has yielded confusing results (Breathnach, Carrington & Black, 1981; Glinski et al., 1978; Wahba et al., 1979; Tagami & Ofuji, 1976; Kruegar, Hill & Jederberg, 1978; Silny et al., 1980; Bloomfield & Young, 1983; Preissner, Schroder & Christophers, 1983). Sampling error may be partly to blame. Peripheral blood neutrophils are a subpopulation, not necessarily representative of the majority which have sequestered in the bone marrow and other tissues, including psoriatic skin. Examination of function of neutrophils in situ in involved or uninvolved skin may prove a better approach (Breathnach et al., 1981; Dubertret et al., 1982). The balance of histological evidence suggests a key role for neutrophils in the pathogenesis of psoriasis, and also poses two important questions. What is the nature of the chemoattractant activity which causes accumulation of neutrophils in the epidermis? How does the presence of activated neutrophils in the epidermis infiuence keratinocyte growth and differentiation? A number of authors have demonstrated leukocytic chemotactic activity in psoriasis scale (Langhof & Muller, 1966; Tagami & Ofuji, 1976, i977)Tagami and Ofuji prepared aqueous