| Popis: |
Background: The undesirable effects of prolonged tobacco use and cigarette smoking are well-known and are due to inhalation of a great number of alkaloids including nicotine. Lung cancer is the most feared ailment in chronic smokers and its linkage with nicotine is not always justified. Notably, it has been shown that nicotine possesses anti-inflammatory properties and considering the link between chronic inflammation and cancer it is conceivable to assume that nicotine may reduce tumorigenesis. Our task was to examine the capacity of nicotine to promote peripheral blood mononuclear cells (PBMC) for cytokine production and to assess its ability to modify the cross-talk between immune and colon cancer cells. Methods: Unstimulated and LPS stimulated PBMC were incubated with various concentrations of nicotine and the generation of the cytokines TNFα, IL-1β, IL-6, IFNγ, IL-2, IL-10, and IL-1ra was detected. In addition, the production of these cytokines was examined in co-cultures of PBMC with HT-29 or RKO colon carcinoma cells in the presence of nicotine. Results: Nicotine caused inhibition of TNFα, IL-6, IL-1β and IL-1ra secretion by non-stimulated PBMC and reduced IL-6 and IFNγ production by mitogen stimulated cells. The effect of nicotine on the immune function of PBMC became prominent when the cells were triggered for cytokine production by HT-29 colon carcinoma cells. The secretion of the pro-inflammatory cytokines TNFα, IL-1β, IL-2 and IFNγ was inhibited, whereas that of IL-6 was not affected. Cytokine production by PBMC induced by RKO cells was not affected by nicotine at any of the concentrations used, suggesting cell-specific immune response. Conclusion: Nicotine inhibited the production of proinflammatory cytokines by PBMC. This effect was more conspicuous when PBMC were promoted by HT-29 colon carcinoma cells. It is feasible that nicotine, acting as an anti-inflammatory agent, may modulate the cross-talk between immune and cancer cells and to delay the progress of carcinogenesis. |
