Abstract
BackgroundPyocyanin (PCN), an extracellular product of Pseudomonas aeruginosa and a blue redox active secondary metabolite, plays an important role in invasive pulmonary infection. However, the detailed inflammatory response triggered by PCN infection in inflammatory cells (particularly macrophages), if present, remains to be clarified. To investigate the effects of PCN on macrophages, the ability of PCN to induce inflammation reaction and the signaling pathway for IL-8 release in PCN-induced differentiated U937 cells were examined.ResultsIt was found that PCN increased IL-8 release and mRNA expression in Phorbol 12-myristate 13-acetate (PMA) differentiated U937 cells in both a concentration- and time-dependent manner by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). P38 and ERK MAPKs were activated after 10 min of induction with PCN and their levels returned to baselines after 30 min by Western blotting. It was also found that within 10 min of PCN incubation, the level of p-I-κBα in the cytosol was increased, which returned to baseline level after 60 min. Meanwhile, the level of p-p65 was increased in the nuclear extract and cytosol, and maintained high in total cell lysates. The results were further confirmed by the observation that p38, ERK1/2 and NF-κB inhibitors inhibited PCN-induced NF-κB activation and attenuated PCN-induced IL-8 expression in U937 cells as a function of their concentrations. Moreover, it was shown that PCN induced oxidative stress in U937 cells and N-acetyl cysteine, an antioxidant, was able to inhibit PCN-induced IL-8 protein expression.ConclusionsIt is concluded that PCN induces IL-8 secretion and mRNA expression in PMA-differentiated U937 cells in a concentration- and time- dependent manner. Furthermore, p38 and ERK MAPKs and NF-κΒ signaling pathways may be involved in the expression of IL-8 in PCN-incubated PMA-differentiated U937 cells.
Highlights
Pyocyanin (PCN), an extracellular product of Pseudomonas aeruginosa and a blue redox active secondary metabolite, plays an important role in invasive pulmonary infection
The results showed that PD98059 and SB203580 significantly decreased the secretion of IL-8, and as either substance’s concentration increased, IL-8 secretion decreased, indicating that PCN may stimulate U937 cells to express IL8 by both MAP kinase (MAPK) signaling pathways (Figure 3)
The present study extends these findings by demonstrating that MAPKs and nuclear factorκB (NF-κB) signalings lie behind PCN-induced IL-8 production in differentiated U937 cells
Summary
Pyocyanin (PCN), an extracellular product of Pseudomonas aeruginosa and a blue redox active secondary metabolite, plays an important role in invasive pulmonary infection. The detailed inflammatory response triggered by PCN infection in inflammatory cells ( macrophages), if present, remains to be clarified. Pseudomonas aeruginosa (P. aeruginosa), an opportunistic pathogen, causes infections associated with high incidences of morbidity and mortality in immunocompromised hosts. The redox-active phenazine PCN, a blue redox active secondary metabolite, plays an important role in invasive pulmonary infection. Studies have shown that PCN causes multiple effects on human cells, such as inhibition of cell respiration, ciliary function, epidermal cell growth, and prostacyclin release. PCN alters calcium homeostasis, causing damage to human cells. Recent studies have confirmed that PCN can alter the host’s immune response and increase IL-1 and TNF-α secretion induced by monocytes
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