Toll-like receptor 7 deficiency mitigates hyperoxia-induced acute lung injury in mice.

INTRODUCTION:Toll-like receptor (TLR) 7 is an important mediator in inflammation. However, its role in hyperoxia-induced acute lung injury (HALI) remains to be elucidated. METHODS:C57BL/6 wild-type and C57BL/6 background TLR 7 deficiency mice were exposed to hyperoxia to stimulate HALI in airtight cages. Animals were sacrificed at 72 h post hyperoxia or room air exposure. Lung injury indicators were measured. Moreover, soluble epoxide hydrolase (sEH) activity was detected by a 14, 15-EET/DHET ELISA kit. Activation of activator protein (AP)-1 and nuclear factor kappa-B (NF-κB) was detected with enzyme linked immunosorbent assay kits. RESULTS:Our data revealed that pulmonary histological assay and wet to dry weight ratio, myeloperoxidase and malondialdehyde activity were reduced in TLR 7 deficiency mice compared with wild-type mice. Moreover, hyperoxia-caused elevation of sEH activity was reduced in TLR 7 deficiency mice. Transcription factors AP-1 activation was significantly inhibited in TLR 7 deficiency mice compared with wild-type mice. Similarly, the activation of NF-κB was reduced in TLR 7 deficiency mice. Tumor necrosis factor-α and interleukin-1β, potent proinflammatory cytokines, were reduced in TLR 7 deficiency mice. CONCLUSION:TLR 7 deficiency is associated with inhibition of inflammation in HALI in mice.

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