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[Expression of TLR3 and IL-8, Eotaxin in the airway smooth muscle cells induced by PolyI:C]
Ming-Hua Yan1, Shu-Yang Zhu, Cun-Ling Duan
1Department of Respiratory Medicine, the Affiliated Hospital of Xuzhou Medical College, Xuzhou 221002, China. jiechenz356@sodu.com
Aim:
to observe the effect of PolyI:C on the expression of TLR3 and inflammation cytokine in the airway smooth muscle cells ASMCs of rat, to investigate relationship between the expression of Toll-like receptor 3 (TLR3) in the airway smooth muscle cells and airway inflammation.
Methods:
airway smooth muscle cells were derived from rat airway tissue and were cultured in vitro, ASMCs were divided into 2 groups: control group and PolyI:C group, PolyI:C group was divided into the different time spots. The mRNA expression of TLR3 was measured by RT-PCR. The level of NF-kappaB was measured by Western blot. The concertration of IL-8 and Eotaxin in ASMCs supernatant were determined by ELISA.
Results:
the expression of TLR3 mRNA and NF-kappaB protein in the ASMCs in PolyI:C group was significantly higher than those in control group(P<0.05), the concentration of IL-8 and Eotaxin in the ASMCs in PolyI:C group was significantly higher compared to control group (P<0.05); and have time dependent manner.
Conclusion:
poly I:C promoted the expression of TLR3 in ASMCs, activated NF-kappaB, incresead the concentration of IL-8 and Eotaxin, involved in airway inflammation of asthma.
Insights
Polyinosinic:polycytidylic acid (PolyI:C) increases Toll-like receptor 3 (TLR3) expression and inflammatory cytokines in rat airway smooth muscle cells. This suggests PolyI:C plays a role in airway inflammation.
Area of Science:
- Immunology
- Cell Biology
- Respiratory Medicine
Background:
- Airway smooth muscle cells (ASMCs) play a role in airway inflammation.
- Toll-like receptor 3 (TLR3) is implicated in inflammatory responses.
Purpose of the Study:
- To investigate the effect of PolyI:C on TLR3 expression and inflammatory cytokines in rat ASMCs.
- To explore the relationship between TLR3 expression in ASMCs and airway inflammation.
Main Methods:
- ASMCs were cultured in vitro and divided into control and PolyI:C groups.
- TLR3 mRNA expression was measured by RT-PCR.
- NF-kappaB protein levels and IL-8 and Eotaxin concentrations were determined by Western blot and ELISA, respectively.
Main Results:
- PolyI:C significantly upregulated TLR3 mRNA and NF-kappaB protein expression in ASMCs compared to controls (P<0.05).
- Concentrations of IL-8 and Eotaxin were significantly elevated in the PolyI:C group, showing a time-dependent increase (P<0.05).
Conclusions:
- PolyI:C promotes TLR3 expression and activates NF-kappaB in ASMCs.
- PolyI:C increases IL-8 and Eotaxin, contributing to airway inflammation, potentially in asthma pathogenesis.
