Absence of regulation of human polymorphonuclear oxidative burst by interleukin-10, interleukin-4, interleukin-13 and transforming growth factor-betain whole blood

Cytokines such as IL-10, IL-4, IL-13 and TGF-beta play a major role in the regulation of immune responses and are considered as anti-inflammatory agen ts mainly due to their actions on monocytes. These cytokines are also known to participate in the regulation of PMN activities. However, few and contr adictory results have been reported on their direct and priming effects on the PMN oxidative burst, which is essential for killing bacteria. We used a flow cytometry method to study the effects of these cytokines on the PMN o xidative burst; we also used whole blood to avoid PMN activation related to isolation procedures and in order to simulate the in who situation more cl osely. None of the cytokines tested had direct or priming effects on PMN H2 O2 production. We also show for the first time that these cytokines do not modulate TNF priming of the PMN oxidative burst in response to N-formyl pep tides (fMLP). These results show that the anti-bacterial activity of PMN, i n terms of the PMN respiratory burst, is not down regulated by these anti-i nflammatory cytokines in whole blood.