The Effect of Melatonin or Luzindole on OVA-Induced Airway Inflammation
Another important question arises whether endogenous melatonin increased by TLR2 deficiency directly suppresses NLRP3 inflammasome activity or feedback controls TLR2-NLRP3 signal. To address this question, melatonin or its receptor antagonist luzindole was applied as illustrated in Figure 4A. First, we found that administration of melatonin significantly attenuated the protein level of OVA-induced TLR2 in WT mice (Figures 4B,C). Meanwhile, melatonin-treated mice showed reductions in leukocyte recruitment and mucus productions compared with vehicle-treated WT mice post OVA challenge (Figures 4D–G). However, administration of luzindole only significantly promoted mucus productions in comparison with vehicle-treated TLR2−/− mice post OVA challenge (Figures 4D–G).
Figure 4  The effect of melatonin or luzindole on OVA-induced airway inflammation. (A) Protocol of administration of melatonin or luzindole during establishing allergic airway diseases model. (B,C) Protein expression of TLR2 in lung tissues of OVA-challenged WT mice treated with melatonin or not. (D) Lung histopathology based on H&E staining to evaluate inflammatory cell infiltration, arrows indicates infiltrated leukocytes. (E) Mucus secretion was analyzed based on PAS staining, arrow heads indicates goblet cells. (F) Histological scoring of lung inflammation. (G) Quantification of mucus secretion. *p < 0.05, **p < 0.01, ***p < 0.001.