[Relationship between mitochondrial cytochrome oxidase mRNA expression and maternal inheritance of asthma]

To explore the relationship between the mRNA expression level of mitochondrial cytochrome oxidase and the maternal inheritance of asthma.

From January to December 2009, 220 asthma patients, 162 patient kins and 260 healthy subjects were recruited from Departments of Respiratory Critical Care Medicine and Pediatric Medicine at First Affiliated Hospital, Kunming Medical College. Lung function tests were performed and serum IgE level measured. The polymorphism of mitochondrial cytochrome oxidase gene polymorphisms was detected by direct sequencing. And the peripheral level of COX mRNA was measured by reverse transcription-polymerase chain reaction (RT-PCR).

No significant difference existed in age, gender among 3 groups. For 3 groups, the first second forced expiratory volume (FEV1)/forced vital capacity (FVC) were 90.6 ± 6.2, 92.3 ± 2.3, 102.3 ± 2.3 and FEV1 percentage of expected value (FEV1%) were (82.9 ± 10.8)%, (94.8 ± 5.4)% and (98.3 ± 8.6)% respectively. The lung function was not significant difference among three groups. The mRNA expression level of mitochondrial cytochrome oxidase in peripheral blood were 0.357 ± 0.217, 0.637 ± 0.473 and 0.975 ± 0.260 in the asthma, kin and control groups respectively. No significant difference existed in the expression level of COX3 mRNA among 3 groups (F = 21.45, P = 0.012). The serum level of lgE was the highest for the asthma patients. And it was significantly higher in the asthma group than that in the control group ((283.6 ± 62.4) vs (52.3 ± 13.7) µg/L, F = 48.31, P < 0.05). Moreover, the serum level of IgE was significantly higher in the kin group than that in the control group ((116.4 ± 57.5) vs (52.3 ± 13.7) µg/L, F = 20.45, P < 0.05). However, there was a negative correlation between the mRNA expression level of mitochondrial cytochrome oxidase and the serum level of IgE among 3 groups.

The down-regulated mRNA expressin of mitochondrial cytochrome oxidase may participate in allergic inflammation by regulating the level of IgE. And the maternal inheritance of asthma is in effect.