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monocyte-derived macrophages to kill ingested Staphylococcus aureus and to promote the release of lymphokines associated with cellular immune functions. The extract induced the proliferation of THP-1 cells within one day of exposure to quantities normally associated with phytohaemagglutinin [29].
2.2. Immunomodulatory activity of plant derived compounds 2.2.1. Sterols and sterolins The phytosterols, β-sitosterol, and its glucoside (Fig. 2) enhanced the in vitro proliferative response of T-cells stimulated by sub-optimal concentrations of phytohaemagglutinin several fold at extremely low concentrations (femtogram level). A 100:1 (mass:mass) ratio of β-sitosterol: β-sitosterol glucoside showed higher stimulation than the individual sterols at the same concentration [30]. The mixture of the sterols (β-sitosterol) and sterolins (β-sitosterol glucoside) has the ability to enhance the cellular response of T lymphocytes both in vitro and in vivo. The mixture enhances the cytotoxic ability of natural killer (NK) cells against the target cancer cell line NK562. It has also been postulated that the sterol-sterolin mixture in a specific ratio could reinstate a balance between the TH1–TH2 cells, a delicate balance that determines the final outcome of an immune response. The same mixture inhibited the release of pro-inflammatory cytokines from endotoxin activated monocytes: interleukin-6 and tumour necrosis factor-α secretion [31]. In HIV-infected patients analysis of the CD4 cell-type (TH1 vs TH2-type) showed that those receiving the sterol-sterolin mixture maintained a favorable TH1 response, which implies that their cell-mediated response was possibly responsible for the viral control and inhibition of CD4 cell loss [32]. However, the cellular target of these molecules was not clearly described cytoplasmic receptors, gene regulation. In a different study, the total cells and eosinophils in the bronchoalveolar lavage fluid markedly decreased after β-sitosterol and lactose-β-sitosterol administration. They also mitigated the inflammation by eosinophil infiltration and mucus hypersecretion by goblet hyperplasia, inhibited the increased mRNA and protein expression of IL-4 and Et
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Figure 2. β-sitosterol and β-sitosterol glucoside.
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