• Preventive Nutrition and Food Science
• /
• v.10 no.2
• /
• pp.161-166
• /
• 2005

We investigated the effect of pycnogenol (PYC) supplementation on retarding the immune dysfunction of CS7BL/6 mice after murine AIDS (MAIDS) development. Dysfunction of T and B cell mitogenesis from primary cultured splenocytes has been observed with retrovirus infection and PYC supplementation partially recovered the dysfunction of T and B cells. There was an abnormal shift of cytokine pattern with retrovirns infection, which was designated by the decreased secretion of Th1 cytokines and increased secretion of Th2 cytokines. PYC supplementation increased IL-2 and $IFN-\gamma$ secretion and decreased IL-4, IL-6, and $TNF-\alpha$ secretion, but it was not sufficient enough to maintain the normal level of these cytokines. Hepatic vitamin E level was significantly decreased by retrovirns infection, in accordance with increased hepatic lipid peroxidation level, whereas PYC supplementation normalized the hepatic level of vitamin E and lipid peroxidation. This study suggests that PYC supplementation may partially help retard the incidence of symptoms during MAIDS.

• YAKHAK HOEJI
• /
• v.39 no.6
• /
• pp.585-592
• /
• 1995

Soil microorganisms producing immunomoduators that can restore ultraviolet B (UVB) radiation-induced suppression of the immune response were screened in vitro. Exposure of freshly isolated murine epidermal cells (EC) to $180{\;}J/m^{2}$ of UVB radiation resulted in approximately 90% impairtnent of accessory cell function, as measured by their ability to support anti-CD3 monoclonal antibody-induced T-cell mitogenesis. When the culture supenmtants of 150 actinomycete strains were exanuned for their capacity to prevent or repair the UVB-induced impairment of accessory cell function, 4 of them were identified to contain immunomodulators that can restore the decreased accessory cell finiction. The soil isolate that showed the most effective restorative activity, G40025. was selected and fturther characters Addition of 10.mu.l of the culture supernatant of G40025 grown in G-media to cultures of UVB-irradiated EC right after UVB-irradiation restored the decreased accessory cell function by 58%. The immunomodtdator produced by G40025 appeared to be stable at 100.deg. C for 10 min. Taxonomical studies by cultural, morphological, and physiological characterization showed that the soil isolate, G40025, belongs to the genus Streptomyces.

• The Korean Journal of Physiology and Pharmacology
• /
• v.4 no.6
• /
• pp.507-513
• /
• 2000

ErbB3/HER3 is a cell surface receptor which belongs to the ErbB/HER subfamily of receptor protein tyrosine kinases. When expressed in NIH/3T3 cells, ErbB3 can form heterodimeric coreceptor with endogenous ErbB2. Among known intracellular effectors of the ErbB2/ErbB3 are mitogen-activated protein kinase (MAPK) and phosphoinositide (PI) 3-kinase. In the present study, we studied relative contributions of above two distinct signaling pathways to the heregulin-induced mitogenic response via activated ErbB3. For this, clonal NIH-3T3 cell lines expressing wild-type ErbB3 and ErbB3 mutants were stimulated with $heregulin{\beta}_1$. While cyclin D1 level was markedly high and further increased by treatment of heregulin in cells expressing wild-type ErbB3, the elimination of either Shc binding or PI 3-kinase binding lowered both levels. This result was supported by the reduction of cyclin $D_1$ expression by preteatment with MAPK kinase inhibitor or PI 3-kinase inhibitor before stimulation with heregulin. In accordance with the cyclin $D_1$ expression, elimination of either Shc binding or PI 3-kinase binding reduced the heregulin-induced DNA synthesis and cell growth rate. Our results obtained by the comparison of wild-type and ErbB3 mutants indicate that the full induction of the cell cycle progression through $G_1/S$ phase by ErbB3 activation is dependent on both Shc/MAPK and PI 3-kinase signal transduction pathways.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.35 no.10
• /
• pp.1329-1335
• /
• 2006

LP-BM5 murine leukemia retrovirus induces the excessive oxidative stress and immune dysfunction leading to B cell leukemia and murine AIDS with cytokine dysfunction. In the present study, the immune restoratory effect of antioxidant hormone dedydroepiandrosterone sulfate (DHEAS) was investigated in the primary splenocytes from LP-BM5 retrovirus-infected C57BL/6 mice. DHEAS significantly increased T and B cell response to mitogen and normalized the unbalanced production of Th1/Th2 type cytokines. In particular, both protein and mRNA expression of IL-4, IL-6, and $TNF-\alpha$ were down-regulated by DHEAS treatment whereas IL-2 and $IFN-\gamma$ level were increased. This result suggests that DHEAS directly or indirectly regulates the gene expression of Th1/Th2 type cytokines in transcription level. In addition, DHEAS treatment decreased the hepatic lipid peroxidation and preserved vitamin E level in liver cells. These results suggested that DHEAS could effectively prevent immune dysfunction by regulating cytokine secretion and preventing the oxidative stress in murine AIDS.