Effects of Steroid Hormones on Human Polymorphonuclear Leukocyte Lysosomes

Persellin, Robert H.; Ku, Leighton

doi:10.1172/jci107832

Cited by 52 publications

(18 citation statements)

References 28 publications

(29 reference statements)

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“…In agreement with our in vivo studies, Persillin and Ku have recently shown failure of steroids to stabilize human lysosomes in vitro (13). The in vitro effects of steroids on the stabilization of liver lysosomes have been questioned (31), and probably will vary with steroid concentration, species, method of preparation, and method of injuring the membranes (32).…”

Section: Additional Studiessupporting

confidence: 81%

See 1 more Smart Citation

The mechanism of action of a single dose of methylprednisolone on acute inflammation in vivo.

Wiener¹,

Wiener²,

Urivetzky³

et al. 1975

J. Clin. Invest.

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Section: Additional Studiessupporting

confidence: 81%

“…In vitro studies have failed to show steroid protection of human neutrophil lysosomal membranes from thermal or detergent injury (13).…”

Section: Introductionmentioning

confidence: 99%

The mechanism of action of a single dose of methylprednisolone on acute inflammation in vivo.

Wiener¹,

Wiener²,

Urivetzky³

et al. 1975

J. Clin. Invest.

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“…The anti-inflammatory action of corticosteroids is thought to be mediated in part by stabilization of plasma and lysosomal membranes (16), although studies with phagocytic cells and bactericidal systems have failed to support this concept (17,18). The inhibition of arachidonic acid release by corticosteroids could result from stabilization of the cellular membranes, thereby rendering the phospholipids less accessible to phospholipases; however, the inhibition of release could also result directly from inhibition of phospholipase activity or indirectly from the corticosteroids' effect on cellular metabolism.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of arachidonic acid release from cells as the biochemical action of anti-inflammatory corticosteroids.

Hong¹,

Levine²

1976

Proc. Natl. Acad. Sci. U.S.A.

487

104

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Serum stimulates the production of prostaglandins by transformed mouse fibroblasts. Hydrocortisone (cortisol) inhibits this stimulation. The half-maximal inhibition occurs at 6 X 10-9 M. Studies with cells labeled with [3Hlara-chidonic acid in their lipids show that the stimulation by serum results in the release of arachidonic acid from the cellular lipids, mostly phospholipids. Hydrocortisone inhibits this release but does not inhibit the production of prostaglandins from exogenously supplied arachidonic acid. This inhibition of arachidonic acid release from phospholipids may be the mechanism for the anti-inflammatory action of corticosteroids. Prostaglandins E2 and F2a (PGE2 and PGF2a) are present in the culture medium of a methylcholanthrene-transformed mouse fibroblast, MC5-5 (1, 2). This cell line proves to be a useful model for the study of the effect of vasoactive substances on the production of prostaglandins. We have shown that mechanical manipulation and vasoactive substances such as bradykinin, arachidonic acid, serum, and thrombin stimulate the production of prostaglandins. Cofactors for in vitro microsomal prostaglandin synthetase systems, such as hydroquinone and glutathione, also stimulate prostaglandin synthesis by the cells. Indomethacin, a nonsteroid anti-inflammatory drug, inhibited all of the above-mentioned stimulations of prostaglandin formation.Prostaglandins have been implicated in inflammation (3). Nonsteroid, aspirin-like anti-inflammatory drugs such as aspirin and indomethacin inhibit in vitro microsomal prostaglandin biosynthesis, and this inhibition has been postulated to be the basis of their therapeutic effects (4). On the other hand, hydrocortisone (cortisol), an anti-inflammatory steroid, did not inhibit in vitro prostaglandin synthetase systems in some studies (4, 5); but in another study fluocinolone, at high concentrations, did inhibit (6). Corticosteroids do inhibit prostaglandin formation by mouse fibrosarcoma cells (7) and by rheumatoid synovia (8). Lewis and Piper, based on their study on the infusion of adrenocorticotropic hormone into rabbit adipose depots, concluded that inhibition of release of prostaglandins from the tissue was the mechanism of some actions of corticosteroids in inflammation, in gastric mucosa, and in the central nervous system (9). Gryglewski et al. (10), working with perfused guinea pig lungs, suggested that corticosteroids act by reducing the availability of the substrate for the prostaglandin synthetase.The mechanism involving inhibition of release would be less likely if tissue storage of prostaglandins were low, as has been suggested by Ramwell and Shaw (11). In this paper, we report studies on the effect of hydrocortisone on prostaglandin synthesis in MC5-5 cells and provide evidence for the mechanism of the action of corticosteroids in inhibiting prostaglandin synthesis.Abbreviations: PGE2, prostaglandin E2; PGF2a, prostaglandin F2a. MATERIALS AND METHODSCell and Cell Culture. MC5-5, a methylcholanthrenetransformed mouse BALB/3T3 cell...

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“…5 Secondly, cortisol helps the body defend itself against infectious agents (which may occur as a result of attack) by stabilising the membranes of lysosomes. [42][43][44] This improves their ability to engulf foreign species that have been brought into the cell by phagocytosis. The lysosome then undergoes enzymatic responses that reduce its pH so that it can necrose the engulfed infectious agent, contributing directly to the immune response to infection.…”

Section: How Cortisol Enhances Survival: the "Saving" Role Of Stressmentioning

confidence: 99%

Neurobiological Pathways between Chronic Stress and Depression: Dysregulated Adaptive Mechanisms?

Sharpley

2009

Clinical Medicine Insights: Psychiatry

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Stress-related diseases have been predicted to become major contributors to the Global Disease Burden within the next 20 years. Of these, depression is one of the principal identifiable sources of concern for public mental health, and has been hypothesized to be an outcome of prolonged stress. Examination of the hyper-responsiveness of the Hypothalamic-Pituitary-Adrenal axis, consequent elevated serum cortisol, plus the effects of this upon brain structure and function, provides a model for understanding how chronic stress may be a causal vector in the development of depression. Evidence from studies of the effectiveness of antidepressants aimed at reducing cortisol within depressed patients supports this model and suggests avenues for future research and treatment of stress-induced depression.

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Effects of Steroid Hormones on Human Polymorphonuclear Leukocyte Lysosomes

Cited by 52 publications

References 28 publications

The mechanism of action of a single dose of methylprednisolone on acute inflammation in vivo.

The mechanism of action of a single dose of methylprednisolone on acute inflammation in vivo.

Inhibition of arachidonic acid release from cells as the biochemical action of anti-inflammatory corticosteroids.

Neurobiological Pathways between Chronic Stress and Depression: Dysregulated Adaptive Mechanisms?

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