| Bronchial asthma is a widespread chronic disease to children and is a world problem , the prevalence rate have been increasing recently years. The pathogenesis is very complicated and poorly understand now, so extensive study for it in the global so as to explore new and useful pathways for preventing and treatment.Asthma is a chronic inflammation of airway caused by Eosinophil mainly and many inflammatory7 mediators. Airway hyperresponsivenes (AHR)is a main characteristic in asthmatic patients. Recently, a close attention to the neurogenic inflammation in airway which mediated by sensory neuropeptides secreted by sensory nerve and open a new pathway to study it's pathogenesis in asthma.The sensory neuropeptides are localized unmyelinated sensory nerves in the airways,and are the important transmitter of non-adrenergic non-cholinergic(NANC) nerves in the lung. Some sensory neuropeptides have been extensivly studied and show they may be ontribute to asthma, such as Neurokinin A (NKA) .Neurokinin B (NKB) and Substance P (SP).These sensory neuropeptides are released by axon reflexes from sensory nerve endings. The effects of sensory neuropeptides includeSmooth muscle contraction, vasodilatation and oedema, mucus secretion, inflammatory cell activation and act on AHR.The studies to sensory neuropeptides and asthma are mainly based on animal and in vito, haven't any report on asthmatic children, the factors (can increase or decrease) to NKA, NKB, and SP are still poor understand and need further research.Our study will based on asthmatic children and animals mode, using immunology method to detect the content of NKA, NKB and SP from blood, brofichoalveolar lavage (BALF) and lung tissue; using hybridization in situ and RT-PCP. method to detect the distrbution and content of NKA, NKB and SP mRNA from lung tissue. We also detect the influence about cigarrite smoking, cold air. and glucocorticoid to NKA.NKB and SP. Our data will confirmed the relation about sensory neuropeptides and asthma, and cigarrtte smoking, and cold air, and glucocorticoid .Material and mathods1. Clinical data 36 asthmatic children ( age range 7 month -12 years) were studied. All subjects were final diagnosis and teatment in hospitalization. the severe asthmatic children were 18 case and the mild asthmatic children were 16 case. All subjects hadn't treated with glucocorticoid by vein or take orally befor one week; The control subjects (n= 15) were health children.2. Animal model: The routin ways is that: the guinea pigs were sensitized by exposure to aerosolized ovalbumin (1% wt/vol in 0.9% sterile sodium chloride) on 2 occasions separated by 7 days (the day at 1,4,7), 3 min on each occasion ; the guinea pigs were exposured to aerosolized 2%ovalbumin for 5 min after a further week (the day at 21) to provoke asthma attack .The control were exposure to aerosolized NS in the same time.The guinea pigs of the same conditions were divided (at random) as following: ①Sensitizing in routin ways (as above). ②Repeatedly exposured to aerosolized 2%ovalbumin every other days for 1 week (after the day at 21). ③ Normol control(as above). ④ Repeatedly exposured to cigarete smoking condition (from the day at 7, 2hrs per day, for 2 weeks) . ⑤Repeatedly exposured to cigarete smoking condition (from the day at 21, 2 hrs per day, for 1 weeks). ⑥After sensitizing in routin ways, giving the normal conditions for lweek;⑦After sensitizing in routin ways, repeatedly inhal cold air with a face mask for 1 week( 15min, twice a day ); ⑧After sensitizing in routin ways, inhal methylacetic beclometosone with a face mask (the day at 20,21,22;twice a day)3. Sample collection and disposal:1) 8.0ml blood was collected at the stage of acult attack and their clinical remission of the asthmatic children; place the blood into cold tube ( EDTA and Aprotinin), centrifugation at 4℃,15min, reserve the plasma at -70℃.2) The plasma for survey NKAA NKB and SP need extracted by SEP-pak and then freezing-drying using a lyophilizer.
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