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Context: Alum is thought to induce inflammation resulting in the release of danger signals such as uric acid (UA) which in turn enhances the immune response to an antigen. Hydrogen peroxide (H2O2) is produced as a byproduct in the purine catabolic pathway that leads to the production of UA. In addition, serum nitric oxide (NO) levels are increased in inflammation. Objective: To further explore the mechanism of action of alum, this study was designed to determine the effects of catalase and 1400W on the number of interleukin-4 (IL-4) and interferon-γ (IFN-γ) secreting spleen cells in mice given ovalbumin (OVA) with alum. Materials and methods: Groups of BALB/c mice were injected intraperitoneally with alum + OVA, alum, OVA, catalase, or 1400W. Other groups were treated with catalase or 1400W and given alum + OVA. The number of IL-4 and IFN-γ secreting spleen cells were determined at days 4 and 7 postinjection by enzyme-linked immunosorbent spot (ELISPOT). Results: Catalase and 1400W caused a decrease in the number of IL-4 secreting spleen cells induced by alum + OVA. 1400W caused a decline in the IFN-γ secreting spleen cells induced by alum + OVA. Catalase caused an increase in IFN-γ secreting spleen cells. Discussion and conclusion: It appears that H2O2 and NO are needed for alum-induced production of a T-helper 2 cytokine. NO also appears to be needed, whereas H2O2 appeared to inhibit an alum-induced production of a T-helper 1 cytokine. These results might explain why alum is mainly a promoter of a T-helper 2 response. [ABSTRACT FROM AUTHOR]

In addition to the effects on T lymphocytes, Cyclosporin A can inhibit dendritic cells allostimulatory capacity, but its precise mechanism remains unknown. The data in this study demonstrated that Cyclosporin A has no effect on the expression of major histocompatibility complex class II and costimulatory molecular CD80, CD86, CD40 on matured DC induced by Lipopolysaccharide in vitro, but can up-regulated B7-DC expression on DC in an Interleukin-4-dependent manner, which is associated with reduced allostimulatory ability of DC. Furthermore, Cyclosporin A treatment inhibited production of Interferon-γand TNF-α, Interleukin-12p70, but increased production of the Interleukin-10 of DC. Thus, up-regulated expression of B7-DC may be responsible for Cyclosporin A-mediated inhibitory effects on allostimulatory capacity of DC. [ABSTRACT FROM AUTHOR]

Three-hydroxy-3-methylglutaryl CoA reductase inhibitors, also known as statins, are widely used as the drug of choice for the treatment of hyperlipidemia. However, actions beyond that of simply lowering cholesterol levels have been reported. This study aims at evaluating the effect of atorvastatin on antibody interleukin-4 and γ-interferon production in mice immunized with egg albumin. Antibody levels were determined by an enzyme linked immunosorbent assay and cytokine transcripts by reverse transcriptase–polymerase chain reaction. Results indicated that repeated daily doses of 40 mg/Kg body weight of atorvastatin following immunization suppressed the antibody response in mice to egg albumin. Moreover, a decline in interleukin-4 and γ-interferon transcripts was observed. [ABSTRACT FROM AUTHOR]

In this study, we have investigated the effects of the unicellular-green-algae Chlorella vulgaris on the production of INF-γ, IL-2, IL-4 and IL-10 in normal and Listeria monocytogenes infected mice. Our results demonstrated that in normal/non infected mice, CVE administration produced no effects in the levels of all cytokines studied. However, Listeria monocytogenes infection enhanced the production of INF-γ and IL-2 at 48 and 72 h after the bacteria inoculation. Interestingly, the treatment with five consecutive doses of 50 mg/Kg/day of Chlorella vulgaris given previously to infection, led to further increases in INF-γ and IL-2 levels at 48 and 72 h in relation to the presence of infection alone. No changes in IL-4 and IL-10 production were observed in Listeria monocytogenes and CVE treated/infected mice. These results are in accordance with the literature, which shows that CVE is a biological response modifier that enhances resistance to Listeria monocytogenes through augmentation of IL-2 and IFN-γ. [ABSTRACT FROM AUTHOR]