Tissue Eosinophilia in Hypersensitivity Reactions as revealed by the Human Skin Window

Eidinger, D.; Raff, Manfred; Rose, B.

doi:10.1038/196683a0

Cited by 40 publications

(5 citation statements)

References 12 publications

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“…The adherence of eosinophils in whole blood was significantly (P < 0.001) depressed 4 h after oral administration of 40 mg of prednisone. This effect was transient, however, as evidenced by the fact that adherence was normal at 24 and 48 h (Fig. 6).…”

Section: Resultsmentioning

confidence: 96%

“…Corticosteroids have been known for many years to induce peripheral eosinopenia (23) and have also been shown to reduce the local accumulation of eosinophils at sites of immediate hypersensitivity reactions as measured by skin window (24)(25)(26)(27)(28) and dermal biopsy (29) techniques. Nonetheless, the mechanism(s) of corticosteroid-induced eosinopenia and reduced tissue accumulation remains uncertain.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Corticosteroids on Eosinophil Chemotaxis and Adherence

Altman¹,

Hill²,

Hairfield³

et al. 1981

J. Clin. Invest.

114

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A B S T R A C T Therapeutic doses of corticosteroids frequently induce eosinopenia; however, the mechanism(s) involved remain obscure. To investigate this question, we studied the effects of corticosteroids on eosinophil adherence and migration. Eosinophils from normal donors were prepared by dextran sedimentation and Hypaque gradient centrifugation to 45-96% purity. Adherence was measured by filtration of whole blood and isolated eosinophils through nylon wool columns. Before prednisone administration, adherence was 83.8+3.2% for eosinophils in heparinized blood and 82.1±3.2% for isolated eosinophils. 4 h after oral prednisone administration whole blood eosinophil adherence was reduced to 53.9+10.7%; at 24 and 48 h adherence was normal. In contrast, isolated eosinophils showed no decrease in adherence 4, 24, or 48 h after corticosteroid administration. Similarly, in vitro addition of hydrocortisone to isolated eosinophils at 0.01 and 2.0 mg/ml did not reduce adherence. Eosinophil migration was tested in modified Boyden chambers by "lower-surface" and "leading-front" methods, using zymosan-activated serum and buffered saline to assess chemotactic and random migration, respectively. In vitro incubation of eosinophils with hydrocortisone or methylprednisolone produced a dose-dependent inhibition ofchemotaxis. Using lowersurface methods the minimal concentration effecting substantial inhibition was 0.01 mg/ml for both drugs. At 2.0 mglml hydrocortisone and methylprednisolone inhibited eosinophil chemotaxis 82.6±4.4% and 85.0±3.5%, respectively. Using leadiig-front chemotaxis techniques significant inhibition was detected at 0.001 mg/ml hydrocortisone. Eosinophils incubated and washed free of corticosteroids responded normally to chemoattractants, indicating that the inhibitory effect of these drugs was reversible. HydroAddress reprint requests to Dr. Altman. Received for publication 21 March 1979 and in revised form 18 September 1980. 28 cortisone at 2 mg/ml inhibited random eosinophil migration, although this effect was not apparent at lower concentrations. Corticosteroids did not act as chemotactic factor inactivators and were not toxic as measured by trypan blue exclusion. Eosinophils obtained from donors who had received 40 mg of prednisone orally for four days showed normal chemotactic responses, probably reflecting the fact that the cells were washed free of plasma before testing. In contrast, incubation of eosinophils in plasma from donors who had received a 300-mg bolus of hydrocortisone induced 46.1±4.5% more inhibition of chemotaxis than did incubation in normal plasma. These results indicate that: (a) eosinophil adherence is transiently reduced following in vivo corticosteroid administration, (b) eosinophil chemotaxis is inhibited by both in vitro and in vivo administration of corticosteroids, and (c) the chemotaxis inhibiting effect is nontoxic, cell-directed, dose-dependent and reversible. Inhibition of eosinophil adherence and chemotaxis may in part explain how corticosteroids produce eosinopenia a...

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Section: Resultsmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Effects of Corticosteroids on Eosinophil Chemotaxis and Adherence

Altman¹,

Hill²,

Hairfield³

et al. 1981

J. Clin. Invest.

114

View full text Add to dashboard Cite

show abstract

“…The vascular endothelium must therefore also be involved in the process leading to the final increase in tissue eosinophil density. The number of circulating eosinophils is thought to re present a migratory phase from their origin in the bone marrow to their site of senescence or utilization in various tissues [14], Previously, the accumulation of eosinophils has been specifically attributed to the late-phase response, as pointed out above, and several investigators have noted an increase in eosino phil density during the late phase using skin window or dermal biopsy techniques [15][16][17][18]. We observed that these cells appeared in the 6-hour biopsies in all subjects regardless of whether they had a visual latephase response or not.…”

Section: Discussionmentioning

confidence: 99%

Mast Cells, Tissue Histamine and Eosinophils in Early- and Late-Phase Skin Reactions: Effects of a Single Dose of Prednisolone

Hammarlund

Pipkorn²,

Enerbäck³

1990

Int Arch Allergy Immunol

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Skin prick tests with allergen and histamine were performed on the volar aspect of the forearms in a double-blind, cross-over study with 40 mg of prednisolone and placebo in 16 pollen-allergic subjects. Skin biopsies were taken before any treatment and 15 min (group 1; n = 8) and 6 h (group 2; n =8) after local challenge with allergen, corresponding to the timing of an early- and late-phase reaction. The specimens were used for the histological evaluation of mast cell and eosinophil density as well as for the determination of the histamine and protein content. The size of the induced weal and flare area as well as of any late-phase reaction was determined using digitized planimetry. The single dose of prednisolone, given 2 h prior to challenge, did not affect the size of the weal and flare response. Only 4 of the individuals developed a visible late-phase response. Eosinophils were virtually absent before allergen exposure, but were already present 15 min after allergen challenge, largely associated with the blood vessels, and were numerous at 6 h. There was, however, no relationship between eosinophil density and the presence or extent of any visual late phase. The mast cells/basophils showed a tendency to increase at the 6-hour determination. The infiltration of eosinophils was blocked by the glucocorticoid. This treatment also induced a difference in the mast cell density at the 6-hour determinations, associated with a similar difference in the histamine content of the biopsy specimens. From the present study, we can conclude that the eosinophil infiltration is an early event and can be blocked by a single dose of prednisolone only 2 h after the administration of the glucocorticoid.

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“…The recruitment of eosinophils after antigen challenge in atopie subjects was described by Eidinger et al [31] some 30 years ago on the dermis. Since then, the phenomenon has been confirmed several times in different sites using different techniques [32][33][34][35][36][37].…”

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confidence: 92%