Effect of dexamethasone on mechanisms responsible for regulation of polyclonal B-cell response

Pryjma, J; Hd, Flad; Mytar, B; Ennen, J.; Ernst, Martin

doi:10.1016/0192-0561(89)90108-2

Cited by 5 publications

(2 citation statements)

References 15 publications

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“…These substances are able to modulate the expression of a great variety of genes (Schena and Yamamoto 1988;Hadcock and Malbon, 1988;Seitz et al, 1991;Guptaet al, 1991) including genes for growth factors and specific receptors for growth factors (Papa et al, 1990;Djaldetti et al, 1990;Nishida et al, 1989;Polan et al, 1989;Pryjma et al, 1989;Tobler et al, 1991). In contrast to the effect of LPS, corticosteroids apparently do not drive microglia into more differentiated states but rather "freeze" the cells in their actual stages of maturation (Hatakeyama et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Growth control of cultured microglia

Ganter

Northoff

Männel

et al. 1992

J of Neuroscience Research

236

125

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Microglia, the resident macrophages of the brain, typically react to injuries or chronic diseases with proliferation and expression of differentiated features, such as production of cytokines associated with inflammatory events. Regulation and control of microglial cytokine expression, therefore, is a major focus of scientific interest. It has been shown that GMCSF and Il‐3 are potent mitogens for microglia. Moreover, Il‐3 and other cytokines are products of microglia. It is shown here that interleukin‐1 (Il‐1) as well as tumor necrosis factor (TNFα) increased microglial proliferation in mixed astrocyte‐microglial cultures but had no mitogenic effects on isolated microglia. © Wiley‐Liss, Inc. Lipopolysaccharide (LPS), the bacterial endotoxin, irreversibly inhibited microglial cell division in both mixed astrocyte‐microglial cultures and in isolated microglial cultures. By contrast, the corticosteroids hydrocortisone and aldosterone and the synthetic glucocorticoid dexamethasone reversibly inhibited microglial proliferation. They also antagonized the stimulatory effects of Il‐3 and granulocyte macrophage colony‐stimulating factor (GMCSF). Estradiol and progesterone had no significant effects on mixed cultures but inhibited microglial proliferation in isolated cultures. Conditioned media from mixed cultures, isolated cultures, from the WEHI‐2B cell line, or from fresh (serum‐supplemented) media stimulated microglial proliferation to various extents. In summary, cytokine‐mediated microglial proliferation can be down‐regulated by a variety of steroid hormones. Along with their unimpaired access to brain cells in general, corticosteroids likely maintain an inhibitory tonus on microglial proliferation. It is hypothesized that this inhibition is overcome locally and temporally in brain injury and repair. © Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Growth control of cultured microglia

Ganter

Northoff

Männel

et al. 1992

J of Neuroscience Research

236

125

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“…We have suggested earlier [9,10] that inflammation produced by AdDP or MDP is probably initiated by augmented production of some immunoregulatory/inflammatory cytokines like IL-1, TNF, MIP-1, etc. The suppressive effects of dexamethasone, a well-recognized inhibitor of their production [13][14][15], might indicate that some of these factors could be involved also in formation of edema induced by other derivatives of AdDP, as well as by glutamine and glutamic acid. Suppressive intervention of indomethacin then suggests that these amino acids are able to provide a sufficient stimulatory signal for enhanced production of eicosanoid inflammatory mediators.…”

Section: Discussionmentioning

confidence: 99%

Immune-related edemagenic activity of glutamines and glutamic acid, components of immunomodulatory agents

Zı́dek

1994

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A number of compounds, in their structure similar to the immunomodulatory agent adamantylamide-L-alanyl-D-isoglutamine (AdDP), a desmuramyl analog of muramyl dipeptide (MDP), were compared with respect to their in vivo immunobiological activity. The agents were represented by adamantylamide-peptides or -amino acids differing principally in the nature of glutaminyl moieties. They were all able to induce inflammatory reaction which was prevented by anti-T-cell (TH) mAb, silica, indomethacin and dexamethasone. Responsible for this effect proved to be glutaminyl moieties (glutamine, isoglutamine, or glutamic acid), irrespective of their stereospecificity. Unlike the immunomodulatory molecule of AdDP, neither of the compounds and amino acids were able to stimulate production of antibodies in immunized animals, however.

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