Ethanol inhibits prolactin- and tumor necrosis factor-alpha-, but not gamma interferon-induced expression of intercellular adhesion molecule-1 in human astrocytoma cells.

In humans, alcohol consumption has multiple effects on the immune system. Despite an increase in our understanding of the effects of alcohol on the immune system, little is known about the effect of alcohol on the neuroimmune response. In the central nervous system (CNS), astrocytes and microglial function as immune effector cells.

Ethanol increases the neurotoxic effect of tumor necrosis factor-alpha in cultured rat astrocytes.

Background: The central nervous system is particularly sensitive to the cytotoxic effect of ethanol. In vivo and in vitro studies indicate that ethanol decreases cell proliferation in a number of cells types, including neurons and glial cells in the central nervous system. The cellular mechanisms involved in ethanol-induced cell toxicity, however, are unclear.

Regulation of prolactin receptor expression by estradiol in the female rat brain.

Prolactin (PRL) receptors have been identified in many tissues, including the brain, but little is known about their distribution and regulation. In the female rat brain, ovariectomy significantly (p < 0.05) decreased PRL binding capacity, but not the affinity, in the hypothalamus and pons-medulla.

Prolactin induced expression of glial fibrillary acidic protein and tumor necrosis factor-alpha at a wound site in the rat brain.

To determine if PRL stimulates astrocyte proliferation and cytokine expression in vivo, we examined the effect of PRL on the wound-induced increase in the expression of glial fibrillary acid protein (GFAP) and tumor necrosis factor-alpha (TNF-alpha) in the CNS. Low levels of GFAP detected by Western blot analysis were identified in the non-wounded controls. Five days after the infliction of the wound, the relative abundance of GFAP in the tissue surrounding the wound site was greater than those of intact controls.

Prolactin induced expression of interleukin-1 alpha, tumor necrosis factor-alpha, and transforming growth factor-alpha in cultured astrocytes.

Prolactin (PRL) is a potent mitogen in cultured astrocytes. Because one of the major effects of astrocyte proliferation is the expression of inflammatory cytokines, we examined the effect of PRL-induced mitogenesis on the expression of interleukin-1 (IL-1 alpha), tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor-alpha (TGF-alpha) in cultured astrocytes. Astrocytes were stimulated with PRL or growth hormone (GH), and the expression of cytokines was determined by immunohistochemistry and Western blot analysis.