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  • Title: Melatonin promoted chemotaxins expression in lung epithelial cell stimulated with TNF-alpha.
    Author: Luo F, Liu X, Li S, Liu C, Wang Z.
    Journal: Respir Res; 2004 Nov 10; 5(1):20. PubMed ID: 15537425.
    Abstract:
    BACKGROUND: Patients with asthma demonstrate circadian variations in the airway inflammation and lung function. Pinealectomy reduces the total inflammatory cell number in the asthmatic rat lung. We hypothesize that melatonin, a circadian rhythm regulator, may modulate the circadian inflammatory variations in asthma by stimulating the chemotaxins expression in the lung epithelial cell. METHODS: Lung epithelial cells (A549) were stimulated with melatonin in the presence or absence of TNF-alpha(100 ng/ml). RANTES (Regulated on Activation Normal T-cells Expressed and Secreted) and eotaxin expression were measured using ELISA and real-time RT-PCR, eosinophil chemotactic activity (ECA) released by A549 was measured by eosinophil chemotaxis assay. RESULTS: TNF-alpha increased the expression of RANTES (307.84 +/- 33.56 versus 207.64 +/- 31.27 pg/ml of control, p = 0.025) and eotaxin (108.97 +/- 10.87 versus 54.00 +/- 5.29 pg/ml of control, p = 0.041). Melatonin(10(-10) to 10(-6)M) alone didn't change the expression of RNATES (204.97 +/- 32.56 pg/ml) and eotaxin (55.28 +/- 6.71 pg/ml). However, In the presence of TNF-alpha (100 ng/ml), melatonin promoted RANTES (410.88 +/- 52.03, 483.60 +/- 55.37, 559.92 +/- 75.70, 688.42 +/- 95.32, 766.39 +/- 101.53 pg/ml, treated with 10(-10), 10(-9), 10(-8), 10(-7),10(-6)M melatonin, respectively) and eotaxin (151.95 +/- 13.88, 238.79 +/- 16.81, 361.62 +/- 36.91, 393.66 +/- 44.89, 494.34 +/- 100.95 pg/ml, treated with 10(-10), 10(-9), 10(-8), 10(-7), 10(-6)M melatonin, respectively) expression in a dose dependent manner in A549 cells (compared with TNF-alpha alone, P < 0.05). The increased release of RANTES and eotaxin in A549 cells by above treatment were further confirmed by both real-time RT-PCR and the ECA assay. CONCLUSION: Taken together, our results suggested that melatonin might synergize with pro-inflammatory cytokines to modulate the asthma airway inflammation through promoting the expression of chemotaxins in lung epithelial cell.
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