Suppression of macrophage arming by corticosteroids

Dimitriu, A

doi:10.1016/0008-8749(76)90329-4

Cited by 28 publications

(9 citation statements)

References 17 publications

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“…Evidence accumulates that delayed hypersensitivity can be more easily suppressed by drugs than the antibody response. Apparently the steroids have little effect on the prodtiction of lymphokines, but interfere with their action on effector cell populations (Weston, Klaman & Krueger 1973) Steroids administered in vivo and in vitro altered the capacity of macrophages to be armed (SMAF), and thereby express their cytotoxic potential (Dimitriu 1976). Induced lysosomal stabilization and prevention of enzyme exocytosis (Weissman & Thomas 1962) may account for some of the effects.…”

Section: Discussionmentioning

confidence: 99%

The effect of immunosuppressive agents on periodontal disease in man

Tollefsen

Saltvedt

Koppang

1978

J of Periodontal Research

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Established chronic gingival lessions were studies in four categories of patients. One groups of healthy subjects was kept plaque‐free (CO), while in the second group (CP) moderate accumulations of dental plaque were permitted. The third group (UH) comprised patients with uremia and in hemodialysis. A fourth group (IS) had received renal allografts and was kept on an immunosuppressive regimen. Differential blood counts and serum immunoglobin quantitation from the UH and IS groups gave mean values within normal ranges. Gingival biopsies were obtained from each subject. The connective tissue inflammation (CTI) scores were compared between the groups. Despite abundant local plaque accumulations, the UH group displayed essentially the same CTI scroes as plaque‐free controls (CO), while the IS group showed a significantly lower (p < 0.05) CTI score than the two in question. The CTI scores of the CP group (controls with plaque) were significantly higher (P < 0.01) than those of the UH, IS and CO groups. It is concluded that immunologic homeostasis is important in the periodontal tissue of man.

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Section: Discussionmentioning

confidence: 99%

The effect of immunosuppressive agents on periodontal disease in man

Tollefsen

Saltvedt

Koppang

1978

J of Periodontal Research

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“…Glucocorticoid treatment has been shown to decrease numbers of circulating lymphocytes (Fauci et al, 1976) and T-lymphocyte proliferation (Gillis et al, 1979), and to inhibit macrophage functions and differentiation of monocytes into macrophages (Dimitriu, 1976;Fauci et al, 1976;Snyder & Unanue, 1982;Baybutt & Holsboer, 1990). Further, methylprednisolone has been used as an immunosuppressant in rabbits with renal allografts (Terada & Ueno, 1984;Friedman et al, 1973 Neither of the treated groups shows a significantly altered period of progesterone production; mean progesterone values are not significantly different among the three groups on any day of pseudopregnancy.…”

Section: Discussionmentioning

confidence: 99%

Effect of treatment with methylprednisolone on duration of pseudopregnancy and on macrophages and T lymphocytes in rabbit corpora lutea

Seiner

Schramm²,

Keyes³

1992

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Summary. The potential role of macrophages and T lymphocytes in the destruction of the corpus luteum at the end of the luteal phase was investigated by treating pseudopregnant rabbits with the immunosuppressant glucocorticoid methylprednisolone. Eleven specific pathogen-free New Zealand White rabbits were injected with pregnant mares' serum gonadotrophin (40 iu, i.m.), followed 2 days later by human chorionic gonadotrophin (40 iu, i.v.)

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“…Macrophages have been shown to possess high-affinity binding sites for glucocorticosteroids and to undergo metabolic and functional modulation as a result of both in vivo and in vitro interaction with the steroids. Most of the effects ascribed to the in vitro interaction of glucocorticoids with peritoneal macrophages are of a suppressive nature, i.e., inhibition of cell growth and protein synthesis; decrease of glucose transport and metabolism (Norton and Munck, 1980); inhibition of the production or secretion of elastase, collagenase, and plasminogen activator (Vassalli et al, 1976;Werb, 1978); inhibition of phagocytosis of heatkilled yeast (Grasso et al, 1981(Grasso et al, , 1983, and suppression of macrophage arming by macrophage-activating factors (MAF; Dimitriu, 1976).…”

Section: Shezen Shirmanmentioning

confidence: 99%

Opposing effects of dexamethasone on the clonal growth of granulocyte and macrophage progenitor cells and on the phagocytic capability of mononuclear phagocytes at different stages of differentiation

Shezen

Shirman

Goldman

1985

Journal Cellular Physiology

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Dexamethasone, a synthetic glucocorticosteroid, was shown to modulate the colony-stimulating factor-dependent clonal growth of myeloid progenitor cells in semisolid agar cultures, enhancing the formation of granulocyte colonies (50-100%) and suppressing the formation of macrophage colonies (75-97%). Modulation of the pattern of myeloid colony formation by dexamethasone (12-125 nM) was brought about when the steroid was administered to 6-day cultures at the time of culture initiation and up to 72 hr later. Dexamethasone inhibited myeloid cell proliferation when administered to 5-day liquid cultures at culture initiation and up to 96 hr later. Dexamethasone (12-250 nM) also enhanced the phagocytic activity of bone marrow-derived mononuclear phagocytes toward heat-killed (HK) yeast cells (up to 100%) and IgG-coated sheep red blood cells (up to 60%). Enhancement of the phagocytic capability depended critically on the stage in culture at which dexamethasone was administered. Exposure to dexamethasone for 28 hr up to 96 hr of 96-hr cultures of bone marrow cells did not lead to a modulation of phagocytic activity of the developing mononuclear phagocytes. The presence of dexamethasone during the critical period of 96 hr to 120 hr after culture initiation led to an enhanced phagocytic capability, which was statistically significant already 12 hr after the administration of the glucocorticoid. Dexamethasone induced an enhanced phagocytic activity when administered at any time after culture initiation provided that it was in culture during this critical period. When added at 120 hr of culture, dexamethasone no longer enhanced the phagocytic capability of mononuclear phagocytes and when added later than 156 hr of culture suppressed it. Dexamethasone also suppressed (up to 68%) the phagocytic capability of resident and elicited peritoneal macrophages. The results suggest that glucocorticoids shift the balance of granulocyte vs. macrophage formation at early stages of precursor cell differentiation. Reduction in mononuclear phagocyte growth and enhancement of its phagocytic capability might reflect accelerated differentiation/maturation steps. The inhibitory effect of dexamethasone on macrophage formation and on the phagocytic capability of mature mononuclear phagocytes and peritoneal macrophages might be a relevant aspect of the in vivo immune suppression encountered after glucocorticoid administration.

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Suppression of macrophage arming by corticosteroids

Cited by 28 publications

References 17 publications

The effect of immunosuppressive agents on periodontal disease in man

The effect of immunosuppressive agents on periodontal disease in man

Effect of treatment with methylprednisolone on duration of pseudopregnancy and on macrophages and T lymphocytes in rabbit corpora lutea

Opposing effects of dexamethasone on the clonal growth of granulocyte and macrophage progenitor cells and on the phagocytic capability of mononuclear phagocytes at different stages of differentiation

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