Objective: To study the expression of leukemia inhibitory factor (LIF) and neurokinin receptors (NKR) in the lungs of asthmatic rats, and to evaluate the role of LIF in airway neurogenic inflammation.
Methods: Twenty-four Wistar rats were randomly divided into a control group (group A, n = 8), an asthma group (group B, n = 8) and a dexamethasone treated group (group C, n = 8). The rat asthmatic model was made by intraperitoneal injection and nebulized aspiration of ovalbumin (OVA) at the concentrations of 10% and 1% respectively. Expression levels of lung LIF, NK-1R and NK-2R were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot two weeks after challenge, and the localization of NK-1R was determined by immunohistochemistry.
Results: After challenge, the expressions of lung LIF mRNA in group A, B and C were 0.240 +/- 0.020, 0.510 +/- 0.130, 0.180 +/- 0.050, and protein levels were 23 110 +/- 8 018, 40 832 +/- 12 964, 16 160 +/- 2 108 respectively. The expressions of lung NK-1R mRNA in group A, B and C were 0.240 +/- 0.020, 1.040 +/- 0.480, 0.170 +/- 0.040, and protein levels were 16 538 +/- 4 342, 32 292 +/- 4 564, 15 018 +/- 1 488 respectively. The mRNA and protein levels of LIF and NK-1R in group B were significantly elevated as compared with group A and C (all P < 0.01). The expressions of lung NK-2R mRNA in group A, B and C were 0.240 +/- 0.040, 0.200 +/- 0.030 and 0.210 +/- 0.040, and no difference was found among three groups (all P > 0.05). In group B, there was a positive correlation between LIF and NK-1R at mRNA (r = 0.850, P < 0.01) and protein (r = 0.868, P < 0.01) levels respectively. NK-1R immunoreactivity was observed primarily in bronchial epithelial cells.
Conclusion: LIF and NK-1R were excessively expressed and closely correlated in lungs of the rat asthmatic model, suggesting that LIF may be involved in modulating airway neurogenic inflammation.