To better define the inflammatory infiltrates and kinetics of mediator release during the cutaneous late-phase reaction (LPR), we examined skin biopsies at 8 h, and skin chamber cell counts and mediator release for 12 h after antigen challenge. Compared with the control sites, the antigen-stimulated biopsy sites contained 14 times as many basophils (P < 0.01) and six times as many eosinophils (P < 0.001) with one to two fold more mononuclear cells (P < 0.03) and neutrophils (P < 0.01). Similar changes were found in the skin chambers. Although there were neutrophils in the control chamber, they were only twice as numerous in the antigen challenged site (P < 0.01). Eosinophils were 35-fold (P < 0.03) more prevalent in the antigen chamber than the control chamber for hours [8][9][10][11][12] and basophils were noted starting in the eighth hour and were 20-fold (P < 0.03) more concentrated in the antigen chamber during the next 4 h. The mononuclear cells were not significantly different between antigen and control blisters. With respect to inflammatory mediators, there was an initial peak of histamine (13.2±2.9 ng/ml) in the blister fluid at 1 h. The level then fell to -2 ng/ml, followed by a secondary rise starting at the eighth hour and increasing to 9.8±2.8 ng/ml by the twelfth hour. This secondary increase in histamine correlated significantly (r = 0.81, P < 0.05) with the observed influx of basophils. PGD2 in the blister fluid rose to 371±25 pg/ml during the first 4 h and then slowly decreased to half this level during the last 4 h. Thus, the cutaneous LPR has been shown to manifest a secondary increase in histamine levels and a markedly specific increase in eosinophils and basophils with mediator release apparently being derived from the latter cells.

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