骨髓中表达白细胞介素5受体 mRNA的CD+34 细胞与支气管哮喘气道炎症的关系

目的　探讨支气管哮喘 (简称哮喘 )小鼠骨髓 (BM)中表达CD+ 34 与白细胞介素 5受体(IL 5RmRNA+ )的造血细胞 (CD+ 34 IL 5RmRNA+ 细胞 )在气道炎症中的作用。方法　以卵白蛋白(OVA)及生理盐水致敏并激发Balb/c小鼠 ,建立各哮喘及对照组 (A组 )模型。分别于OVA及生理盐水首次激发后 1、6、12、2 4、48h处死小鼠 ,取支气管肺泡灌洗液 (BALF)、外周血 (PB)及BM标本备用。测定BALF中嗜酸性粒细胞 (EOS)、PB中有核细胞及EOS计数及BM中有核细胞数 ;用流式细胞仪分别测定PB及BM中CD+ 34 细胞占相应有核细胞的比例并推算其相对计数 ;用免疫组化结合原位杂交法分别标记骨髓细胞CD+ 34 抗原及IL 5RmRNA ,定位BM中CD+ 34 IL 5RmRNA+ 细胞并计数其占CD+ 34 细胞的比例。结果　 (1)OVA激发后 6h组 ,BALF中EOS计数为 (2 67± 1 0 0 )× 10 5/L ,与A组 (0 46±0 0 6)× 10 5/L]比较差异有显著性 (P <0 0 1) ;OVA激发后 12h组 ,BALF中EOS、PB中EOS计数分别为 (7 74± 1 98)× 10 5/L、(2 91± 0 64 )× 10 8/L ,与A组 (0 46± 0 0 6)× 10 5/L、(1 43± 0 3 7)× 10 8/L]比较 ,差异有显著性 (P均 <0 0 1) ;OVA激发后 2 4h组 ,BALF中EOS、PB中EOS计数分别为 (19 43±3 69)× 10 5/L、(3 93± 0 5 1)× 10

Bone marrow-derived CD+34 cells expressing interleukin-5 receptor messenger RNA and asthmatic airway inflammation

OBJECTIVE: To study the possible role of bone marrow-derived hematopoietic cells expressing CD(34)(+) and IL-5 receptor messenger RNA (IL-5R mRNA(+)) in asthmatic airway inflammation. METHODS: Balb/c mice were sensitized and challenged by ovalbumin (OVA) to establish the asthmatic model. The control mice were sensitized and exposed to sterile saline. The mice were killed at different time points after challenged by OVA and sterile saline, and bronchoalveolar lavage (BALF), peripheral blood (PB) and bone marrow (BM) were prepared. Eosinophils (EOS) in PB and BALF, and nuclear cells in PB and BM were counted. The percentage of CD(34)(+) cells to nuclear cells (CD(34)(+)%) in PB and BM, and the relative number of CD(34)(+) cells (CD(34)(+)) in PB and BM were calculated by flow cytometry. Immunocytochemistry and in situ hybridization were used to observe the hematopoietic cells with co-localized expression of CD34 and IL-5R mRNA (CD(34)(+)/IL-5R mRNA(+)) in BM. The percentage of BM CD(34)(+)/IL-5R mRNA(+) to BM CD(34)(+) was calculated. RESULTS: (1) At 6 h after OVA challenge, the number of BALF EOS (2.67 +/- 1.00) x 105/L] was significantly increased as compared to the number in controls (0.46 +/- 0.06) x 105/L] (P < 0.01). At 12 h after OVA-challenge, the numbers of BALF EOS (7.74 +/- 1.98) x 105/L] and PB EOS (2.91 +/- 0.64) x 108/L] were significantly higher than those in the controls (P < 0.01). At 24 h after OVA-challenge, the numbers of BALF EOS(19.43 +/- 3.69) x 105/L], PB EOS(3.93 +/- 0.51) x 108/L] and BM CD(34)(+)/IL-5R mRNA(+) (300.50 +/- 90.02) per thousand] were increased to the highest levels. The differences were significant as compared to the corresponding parameters in the controls (P < 0.01). At 48 h after OVA-challenge, the numbers of BALF EOS (12.05 +/- 5.31) x 105/L] and BM CD(34)(+)/IL-5R mRNA(+) (220.80 +/- 53.41) per thousand] were decreased, but were still significantly different compared to the numbers in the controls (P < 0.01), while other markers returned to the normal levels. (2) The number of BM CD(34)(+)/IL-5R mRNA(+) in the 60 mice was closely correlated with BALF EOS, PB EOS, BM CD(34)(+) and BM CD(34)(+) (P < 0.05). CONCLUSION: CD(34)(+) cells expressing IL-5R mRNA, which may favor eosinophilopoiesis and eosinophilic airway inflammation, were increased in the BM of this mouse asthmatic model. A feedback mechanism between the lungs and the bone marrow likely exists, which may be involved in the development and persistence of asthmatic airway inflammation.