Crocin reduces Aspergillus fumigatus-induced airway inflammation and NF-?B signal activation.

Du J1, Chi Y1, Song Z1, Di Q1, Mai Z1, Shi J1, Li M1
Source: J Cell Biochem
Publication Date: ()
Issue: 119: 1746-1754
Cells used in publication:
Epithelial, bronchial (NHBE), human
Species: human
Tissue Origin: lung


Chronic obstructive pulmonary disease (COPD) is a chronic airway inflammation and its exacerbation is often accompanied by Aspergillus fumigatus (A. fumigatus) infection. Increasing evidences demonstrated the potent antioxidant and -inflammatory effects of crocin. However, the role of crocin in A. fumigatus-induced inflammation is still unknown. We aimed to evaluate the role of crocin in inflammation response induced by A. fumigatus in human bronchial epithelial cells and the possible mechanisms. BEAS-2B and NHBE cells were pretreated with crocin for 24?h, and then A. fumigatus conidia were added for 24?h. A. fumigatus treatment exhibited a significant higher TNF-a, IL-8, IL-6, and IL-1ß level (P?<?0.05), whereas crocin pretreatment significantly inhibited A. fumigatus induced the pro-inflammatory cytokines (P?<?0.05). NF-?B inhibitor PDTC inhibited pro-inflammatory cytokines release triggered by A. fumigatus (P?<?0.05). Furthermore, crocin suppressed A. fumigatus induced NF-?B p65 nuclear translocation, the phosphorylation of IKKa and I?Ba, the degradation of I?Ba and NF-?B reporter activity. Crocin pretreatment also resulted in an inhibition of A.fumigatus-induced ROS production (P?<?0.05). Taken together, these results indicate that crocin may prevent A. fumigatus-induced inflammation through suppressing NF-?B signal pathway