Anaphylaxis

Atopic dermatitis: clinical relevance of food hypersensitivity reactions.

Atopic dermatitis and food hypersensitivity reactions.

Previous studies have demonstrated symptoms and mediator release occurring as long as 11 h after nasal challenge with antigen in selected allergic subjects. Pretreatment with systemic steroids reduced symptoms and mediators including histamine, TAME-esterase activity, and kinins. The aims of the present study were to characterize the cell influx during the late-phase response to antigen challenge and to determine the effect of pretreatment with systemic steroids on this response. We examined cytospin slides of nasal washings obtained before and hourly for 11 h after nasal antigen challenge in 10 asymptomatic allergic subjects with a history of seasonal rhinitis and 5 normal, nonallergic subjects. Allergic subjects received oral prednisone (20 mg 3 times a day) or placebo in a random, double-blind crossover manner for 2 days before each of 2 challenges 1 month apart. On placebo days, a mixed cell influx occurred in allergic subjects during the late response that was 50-fold greater than the cell influx in ...

The influx of inflammatory cells into nasal washings during the late response to antigen challenge. Effect of systemic steroid pretreatment.

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 less than 0.01) and six times as many eosinophils (P less than 0.001) with one to two fold more mononuclear cells (P less than 0.03) and neutrophils (P less than or equal to 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 less than 0.01). Eosinophils were 35-fold (P less than or equal to 0.03) more prevalent in the antigen chamber than the control chamber for hours 8-12 and basophils were noted starting in the eighth hour and were 20-fold (P less than or equal to 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 approximately 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 less than 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.

/pdf/cutaneous-late-phase-response-to-allergen-mediator-release-73z4v39r2a.pdf

Cutaneous late-phase response to allergen. Mediator release and inflammatory cell infiltration.

The late phase reaction (LPR), an IgE-dependent sequel to the wheal and flare response (WFR), was studied in ragweed (RW)-sensitive subjects 15 min and 6 to 8 hr after intradermal RW injection. The role of WFR in the genesis of LPR and LPR dependence on RW dose were determined by skin test titration to extinction of LPR. LPR size correlated with WFR size. LPR were noted with WFR as small as 9.5 ± 1.0 mm (S.E.M.) and RW doses as small as 0.01 protein nitrogen unit (PNU). In a group of WFR-positive but LPR-negative subjects, LPR were not induced despite increasing WFR to 18.2 ± 1.3 mm by simultaneous injection of RW + histamine (RW-H). Light microscopy of 1-µm biopsy sections of direct and Prausnitz-Kustner (P-K) LPR revealed a mixed cellular infiltrate qualitatively no different than that seen 6 hr after isolated WFR. Fibrin deposition in the absence of immunoglobulin or complement was seen by fluorescent microscopy in LPR but not in controls. These data suggest that LPR may follow small RW doses. Furthermore, the failure of RW-H injection to induce LPR argues against a gatekeeper role for WFR in the genesis of LPR. The significance of the cellular infiltrate is not clear although fibrin deposition explains the clinical induration of LPR. This fibrin deposition is evidence for activation of the coagulation system in these IgE-dependent “delayed in time” reactions.

The Late Phase Skin Reaction: Evidence for Activation of the Coagulation System in an IgE-Dependent Reaction in Man

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The Late Phase Skin Reaction: Evidence for Activation of the Coagulation System in an IgE-Dependent Reaction in Man