Glucocorticoids and Lysosomes

Eb, Thompson

doi:10.1007/978-3-642-81265-1_31

Cited by 7 publications

(3 citation statements)

References 43 publications

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“…Boxer et al (4), studying the receptors of neutrophils by using a rosetting technique with FITC-conjugated bacteria coated with IgG or C3b, could only detect an effect on the amount of C3b rosettes but not on the number of IgG rosettes. In the present study, we showed that hydrocortisone decreased both the IgGand C3b-mediated interactions with human neutrophils at a hydrocortisone concentration (5 x 10-5 M or higher) which is within probable pharmacological concentrations used in patients (10,13,31,35).…”

Section: Discussionsupporting

confidence: 64%

In vitro effect of hydrocortisone on the attachment and ingestion phases of immunoglobulin G- and complement component 3b-mediated phagocytosis by human neutrophils

Hed¹

1982

Infect Immun

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Section: Discussionsupporting

confidence: 64%

In vitro effect of hydrocortisone on the attachment and ingestion phases of immunoglobulin G- and complement component 3b-mediated phagocytosis by human neutrophils

Hed¹

1982

Infect Immun

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“…They may stabilize lysosomes in vitro especially at high concentrations through direct effects on membranes or, as recently discussed by Thompson (1979), through inhibiting the synthesis of prostaglandins. Disodium cromoglycate is also a direct membrane-stabilizing drug (Orr, 1977).…”

Section: Discussionmentioning

confidence: 97%

Effects of Glucocorticoids and Disodium Cromoglycate on Avidin Production in Chick Tissues

Nordback¹,

Joensuu²,

Tuohimaa³

1982

Journal of Endocrinology

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The effects of anti-inflammatory glucocorticoids and a membrane stabilizer (disodium cromoglycate) on avidin induction were studied. Chicks were primed for 0, 3 or 7 days with diethylstilboestrol (DES; 0.5 mg/day per animal, s.c.). Actinomycin D (0.2 mg/kg, i.p.) stimulated avidin production in the oviduct, intestine, lung and wing muscle of both DES-primed and unprimed chicks. Prednisolone (5 mg/animal, i.m.) given 1 h before actinomycin D reduced the avidin amounts to control levels in the unprimed oviducts and in non-oviductal tissues. The signs of inflammation (ascites, oedema) in chicks receiving actinomycin D also disappeared with prednisolone premedication. Cortisol (50 mg/animal, i.m. or 1, 5 or 50 microgram/ml medium), prednisolone (5 mg/animal, i.m. or 0.5, 5, 10 or 50 microgram/ml medium) and dexamethasone (1 mg/animal, i.m. or 0.05 or 0.5 microgram/ml medium) stimulated avidin production in DES-primed oviducts in vivo and in vitro. Culture in vitro induced avidin production in lung and oviduct but not in wing muscle. This avidin production in culture was not inhibited by cortisol, prednisolone or disodium cromoglycate. It is concluded that actinomycin D induces avidin production through its inflammatory effect and that the induction can be prevented by anti-inflammatory glucocorticoids. It is proposed that the 'spontaneous' avidin production in culture is not the effect of trauma during tissue preparation but rather a new form of avidin induction.

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“…exudation and toxic damages (Jesserer 1973). In this context it was reported about the destruction of lymphocytes, monocytes and eosinophils (Fauci 1979;Harris and Baxter 1979;Spector 1981) as well as about the inhibition of the growth and/or function of neutrophils (Fauci 1979), fibroblasts (Labhart 1978), thymocytes (Baxter and Rousseau 1979) and the stabilisation of lysosomal membranes (Baume and Fiore-Donno 1970;Labhart 1978;Thompson 1979). Up to now, very little is known about the mechanisms of activity, which are altogether based upon the antiphlogistic and immunosuppressive effects.…”

Section: Introductionmentioning

confidence: 96%

Reaction of human leukocytes after in vitro contact with a glucocorticoid

Schmidt¹,

Wagner²

1985

Res. Exp. Med.

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The used hormone prednisolone bisuccinate causes in the concentration range of 2-1,000 micrograms/ml visible changes of the cell morphology and enzymatic activity in all leukocytes. These alterations appear immediately after the application of the glucocorticoid and remain nearly constant during the time of investigation (1 h). The changes in the cell morphology and the loss of enzymatic activity increase with enhanced hormone concentration. The following reproducible morphological changes caused by the hormone comprise swelling, vacuolization and deformation of the nuclei with concomitant release of nuclei material. In addition, cloverleaf and fircone-like structures originate in connection with the formation of small bubbles.

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Glucocorticoids and Lysosomes

Cited by 7 publications

References 43 publications

In vitro effect of hydrocortisone on the attachment and ingestion phases of immunoglobulin G- and complement component 3b-mediated phagocytosis by human neutrophils

In vitro effect of hydrocortisone on the attachment and ingestion phases of immunoglobulin G- and complement component 3b-mediated phagocytosis by human neutrophils

Effects of Glucocorticoids and Disodium Cromoglycate on Avidin Production in Chick Tissues

Reaction of human leukocytes after in vitro contact with a glucocorticoid

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