Effects of Corticosteroid Therapy on Human Monocyte Function

Abstract

Since high-dose corticosteroid therapy appears to impair cellular defense mechanisms, this study examined its effect on human monocyte function. Fifteen normal volunteers were studied before and after a three-day course of prednisone therapy (50 mg every 12 hours for six doses). A transient period of monocytopenia occurred during the first few hours of therapy. Monocyte killing of Staphylococcus aureus was reduced in nine subjects from 5.6 plus or minus 0.2 (plus or minus S.E.) X 10-6 organisms before to 1.3 plus or minus 0.4 x 10-6 organisms at completion of therapy (p less than 0.01). Similary, killing of Candida tropicalis four subjects fell from 9.3 plus or minus 0.6 to 0.6 plus or minus 0.3 x 10-6 organisma (p less than 0.01). Bactericidal activity returned to normal levels 48 hours after the last dose of prednisone. These same monocyte preparations had normal or increased chemotactic response, phagocytic rate of cryptococci, hexosemonophosphate-shunt response to phagocytosis and ultrastructural characteristics. This impairment of bactericidal and fungicidal activity during prednisone therapy may contribute to the infectious complications seen in patients receiving comparable doses of corticosteroids.

Glucocorticoids induced down-regulation of glucocorticoid receptor mRNA expression in asthma

“…None of them had been treated by either inhaled or oral GC for the past 3 months. 2 agonists were used as needed by the asthma symptoms. Six healthy volunteers were also included in this study; they were age-(25-45 years (35 6 5 years)) and sex-(3M/3F) matched.…”

“…Several studies have shown a decrease of cellular infiltration into asthmatic airways following treatment with glucocorticoids (GC) [2]. Generally, GC are able to interfere with the in vivo production of inflammatory mediators to suppress the putative in vivo inflammatory response [3].…”

Peritoneal cavity phagocytes from the teleost sea bass express a glucocorticoid receptor (cloned and sequenced) involved in genomic modulation of the in vitro chemiluminescence response to zymosan

“…In addition, after in vivo or in vitro exposures to GCs, bactericidal and fungicidal ability (Rinehart et al, 1975), cytokine production, MHC class II expression (Snyder and Unanue, 1982) and tumoricidal activity (Hogan and Vogel, 1988;Keil et al, 1995) of humans and murine macrophages were decreased. In vivo, high levels of plasma cortisol produced by stressors can lead to divergent responses including a strong immunosuppressive eVect (Cupps and Fauci, 1982;Rinehart et al, 1975). In Wsh, cortisol (hydrocortisone) is the major corticosteroid with both GC and MC activities.…”

Glucocorticoid induces micro-fat embolism in the rabbit: A scanning electron microscopic study

“…21,22 The dynamics of marrow adipocytes under conditions of corticosteroid administration should be viewed in terms of this differentiation-apoptosis balance 23 and also from the viewpoint of phagocytotic activity. [24][25][26] Regardless of the source of fat globules, we postulated a process of arteriole occlusion once fat globules are formed in the arterial system. The fat globules may initially be very small in size, but can coalesce with ease and become larger.…”