Requirement of Cytokines for Augmentation of the Antigen-Specific Antibody Responses by Ascorbate in Cultured Murine T-Cell-Depleted Splenocytes

Mitsuzumi, Hitoshi; Kusamiya, Makoto; Kurimoto, Takafumi; Yamamoto, Ichiro

doi:10.1254/jjp.78.169

Cited by 17 publications

(9 citation statements)

References 30 publications

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“…The level of intracellular AA-2G was undetectable (<17 ng/10 6 cells) at 2 and 4 days after addition (our unpublished data), suggesting that AA-2G is not efficiently transported into the cells. The time course for depletion of intracellular AA is similar to the time courses reported for murine T-cell-depleted splenocytes and human tonsilar B cells in culture [2,27]. Since ␣-glucosidase activity in the medium supplemented with 10% fetal bovine serum is very low for hydrolysis of AA-2G [22], the conversion of AA-2G to AA may be catalyzed by cellular ␣-glucosidase of B lymphocytes.…”

Section: Discussionsupporting

confidence: 75%

“…The initial intracellular concentration of AA is maintained by exogenous AA added to cultures repeatedly at 12-h intervals but not by single addition of AA because of its instability in the culture medium [2]. Single addition of AA-2G, however, is sufficient to restore and maintain the initial intracellular levels of AA for several days as shown in this study and other studies [27,34]. Thus, AA-2G might be a useful tool for investing the physiological role of AA in long culture systems in vitro.…”

Section: Discussionmentioning

confidence: 64%

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Promotion of IL-4- and IL-5-dependent differentiation of anti-μ-primed B cells by ascorbic acid 2-glucoside

et al. 2009

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The stable ascorbic acid derivative 2-O-alpha-D-glucopyranosyl-L-ascorbic acid (AA-2G) was used to investigate the role of ascorbic acid (AA) in B cell differentiation in vitro. AA-2G is stable in a solution unlike AA but is hydrolyzed by cellular alpha-glucosidase to release AA. Mouse spleen B cells were primed for 2 days with an anti-mu antibody in the presence of interleukin (IL)-4 and IL-5 and then washed and recultured with AA-2G in the presence of IL-4 and IL-5. AA-2G, but not AA, dose-dependently increased IgM production, the greatest enhancement being 150% at concentrations of more than 0.5mM. In the absence of IL-4 and IL-5, primed B cells produced a negligible amount of IgM, and AA-2G had no effect. AA-2G-induced IgM production in the presence of IL-4 and IL-5 was inhibited by the alpha-glucosidase inhibitor castanospermine. Intracellular AA content, depleted during the priming period, increased by adding AA-2G at the start of reculture. Treatment of B cells with AA-2G resulted in an increase in the number of IgM-secreting cells, CD138-positive cells and CD45R/B220-negative cells. The number of viable cells in untreated cultures decreased gradually, but the decrease was significantly attenuated by AA-2G, resulting in about 70% more viable cells in AA-2G-treated cultures. AA-2G caused a slight but reproducible enhancement of DNA synthesis and a slight decrease in the number of cells with a sub-G1 DNA content. These results demonstrated that AA released from AA-2G enhanced cytokine-dependent IgM production in anti-mu-primed B cells and suggest that its effect is caused through promoting the differentiation of B cells to plasma cells and attenuating the gradual decrease in the number of viable cells.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 64%

Promotion of IL-4- and IL-5-dependent differentiation of anti-μ-primed B cells by ascorbic acid 2-glucoside

et al. 2009

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“…Ascorbic acid enhances the human immune response that enhances the Con A-induced proliferation of PBLs [10], chemotaxis of neutrophils [11], and phagocytosis of mononuclear leukocytes [12]. It has been reported that ascorbic acid upregulates the IgM antibody responses in a cytokine-dependent manner in spleenocytes [13]. The in vitro function of endotoxic shock-induced macrophages and lymphocytes was modulated by ascorbic acid [14, 15].…”

Section: Introductionmentioning

confidence: 99%

Immunomodulatory Role ofOcimum gratissimumand Ascorbic Acid against Nicotine-Induced Murine Peritoneal MacrophagesIn Vitro

Mahapatra

Chakraborty

Roy

2011

Oxidative Medicine and Cellular Longevity

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The aim of this present study was to evaluate the immune functions and immune responses in nicotine-induced (10 mM) macrophages and concurrently establish the immunomodulatory role of aqueous extract of Ocimum gratissimum (Ae-Og) and ascorbic acid. In this study, nitrite generations and some phenotype functions by macrophages were studied. Beside that, release of Th1 cytokines (TNF-α, IL-12) and Th2 cytokines (IL-10, TGF-β) was measured by ELISA, and the expression of these cytokines at mRNA level was analyzed by real-time PCR. Ae-Og, at a dose of 10 μg/mL, significantly reduced the nicotine-induced NO generation and iNOSII expression. Similar kinds of response were observed with supplementation of ascorbic acid (0.01 mM). The administration of Ae-Og and ascorbic acid increased the decreased adherence, chemotaxis, phagocytosis, and intracellular killing of bacteria in nicotine-treated macrophages. Ae-Og and ascorbic acid were found to protect the murine peritoneal macrophages through downregulation of Th1 cytokines in nicotine-treated macrophages with concurrent activation of Th2 responses. These findings strongly enhanced our understanding of the molecular mechanism leading to nicotine-induced suppression of immune functions and provide additional rationale for application of anti-inflammatory therapeutic approaches by O. gratissimum and ascorbic acid for different inflammatory disease prevention and treatment during nicotine toxicity.

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“…Many reports have stated that T‐lymphocytes presented CD3 antigen on cell surface membranes are involved in cell‐mediated immunity in cellular immunomodulatory system, and B cells are primarily mediated in humoral immunity (Krop et al,; Mitsuzumi et al,; Lu et al,). Hence, we also examined the cell markers from PBMC of leukemic mice after oral treatment of safrole and our results indicated that the percentages of CD3 (T cells), CD19 (B cells) and Mac‐3 (macrophages) were significantly increased in safrole‐treated leukemic mice, but that the population of CD11b (monocytes) were not significantly affected in leukemic mice after safrole exposure (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…and Table ). It is reported that nonactivated B cells are shown CD19 marker and their differentiation modulate by the interaction of various types of cytokines secreted from macrophages or T cells (Mitsuzumi et al,). Our results showed that safrole could increase B cells (elevated the population of CD19), and the augmenting effect of safrole is carried out through the antibody responses resulted from expansion and differentiation of mainly monocytes and macrophages.…”

Section: Discussionmentioning

confidence: 99%

Safrole suppresses murine myelomonocytic leukemia WEHI-3 cellsin vivo, and stimulates macrophage phagocytosis and natural killer cell cytotoxicity in leukemic mice

Yang

et al. 2011

Environ. Toxicol.

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Many anticancer drugs are obtained from phytochemicals and natural products. However, some phytochemicals have mutagenic effects. Safrole, a component of Piper betle inflorescence, has been reported to be a carcinogen. We have previously reported that safrole induced apoptosis in human oral cancer cells in vitro and inhibited the human oral tumor xenograft growth in vivo. Until now, there is no information addressing if safrole promotes immune responses in vivo. To evaluate whether safrole modulated immune function, BALB/c mice were intraperitoneally injected with murine myelomonocytic WEHI-3 leukemia cells to establish leukemia and then were treated with or without safrole at 4 and 16 mg/kg. Animals were sacrificed after 2 weeks post-treatment with safrole for examining the immune cell populations, phagocytosis of macrophages and the natural killer (NK) cells' cytotoxicity. Results indicated that safrole increased the body weight, and decreased the weights of spleen and liver in leukemic mice. Furthermore, safrole promoted the activities of macrophages phagocytosis and NK cells' cytotoxicity in leukemic mice when compared with untreated leukemic mice. After determining the cell marker population, we found that safrole promoted the levels of CD3 (T cells), CD19 (B cells) and Mac-3 (macrophages), but it did not affect CD11b (monocytes) in leukemic mice. In conclusion, safrole altered the immune modulation and inhibited the leukemia WEHI-3 cells in vivo.

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Requirement of Cytokines for Augmentation of the Antigen-Specific Antibody Responses by Ascorbate in Cultured Murine T-Cell-Depleted Splenocytes

Cited by 17 publications

References 30 publications

Promotion of IL-4- and IL-5-dependent differentiation of anti-μ-primed B cells by ascorbic acid 2-glucoside

Promotion of IL-4- and IL-5-dependent differentiation of anti-μ-primed B cells by ascorbic acid 2-glucoside

Immunomodulatory Role ofOcimum gratissimumand Ascorbic Acid against Nicotine-Induced Murine Peritoneal MacrophagesIn Vitro

Safrole suppresses murine myelomonocytic leukemia WEHI-3 cellsin vivo, and stimulates macrophage phagocytosis and natural killer cell cytotoxicity in leukemic mice

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