Lack of correlation between interleukin 6 and interleukin 1 levels in psoriatic lesional skin.

The histopathologic features of active psoriatic plaques are characterized by epidermal hyperplasia and the presence of inflammatory cells. Recently it has been strongly suggested that an increased local production of cytokines and growth factors by keratinocytes or by activated inflammatory infiltrates play an crucial role in the induction of these changes. Particularly keratinocytes are demonstrated to secrete several different immuno-inflammatory mediators, including interleukin 1 (IL-1), IL-6 and IL-8. IL-1 induces IL-6 production in vitro, which in turn stimulates the proliferation of human keratinocytes. Although IL-1 has been reported to be reduced in samples from psoriatic lesions, enhanced immunohistochemical expression of IL-6 has been shown in psoriatic lesional skin. Thus, we designed the present study to elucidate the paradoxical situation of IL-1 and IL-6 expression in psoriatic skin lesions by directly measuring these cytokines in tissue fluids collected from suction blisters as well as in horny tissue extracts. As reported before, the levels of immunoreactive IL-1-alpha or -1 beta tended to be reduced in the scale extracts of psoriasis and related pustular dermatoses. In contrast, the levels of immunoreactive IL-6 tended to be increased, despite the presence of great variations between samples, a significant elevation being found only in the scale extracts of pustular psoriasis. Although the mean of IL-6 levels in the suction blister fluids from psoriatic involved skin was higher than those from normal or psoriatic uninvolved skin, again no statistical significance was noted. Moreover, no significant correlation was observed between the levels of immunoreactive IL-1 and IL-6 in these materials. Our direct measurements of these cytokines in lesional tissue samples do not provide evidence suggesting any close interrelationship between IL-1 and IL-6 nor provided evidence suggesting a pivotal role for IL-6 in the pathogenetic mechanism of psoriasis.