Allergic eosinophil-rich inflammation develops in lungs and airways of B cell-deficient mice.
Allergic eosinophil-rich inflammation develops in lungs and airways of B cell-deficient mice.
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DOI：
10.1084/jem.185.5.885
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发表时间：
1997-03-03
期刊：
影响因子：
--
通讯作者：
Persson CG
中科院分区：
文献类型：
--
作者：
Korsgren M;Erjefält JS;Korsgren O;Sundler F;Persson CG
免疫球蛋白（IG），特别是IgE，被认为是至关重要的参与哮喘的发病机制，同样，在过敏性模型的疾病。为了验证这一范例，我们检查了纯合突变型C57 BL/6小鼠，它们是B细胞缺陷型，缺乏所有的IG。用10 μg卵清蛋白（OVA）加明矾腹膜内免疫小鼠，然后每天（第14-20天）暴露于OVA气雾剂30分钟（OVA/OVA组）。运行三个对照组：OVA/SAL组：OVA腹腔注射+SAL气雾剂;生理盐水腹腔注射+生理盐水气雾剂;生理盐水腹腔注射+OVA气雾剂（n = 6-7）。在最后一次OVA或SAL暴露后24 h获得的肺和大气道组织通过光学显微镜和透射电子显微镜（TEM）进行检查。接受OVA/ OVA治疗的Ig缺陷小鼠肺肿胀和变色，在大的气道上皮下组织中显示出显著的嗜酸性粒细胞增多（49.2 ± 12.0个细胞/mm基底膜[BM]与OVA/ SAL对照1.2 ± 0.3个细胞/mm BM; P <0.001），以及在肺中的血管周围和支气管周围（49.3 ± 9.0个细胞/单位面积对OVA/SAL对照2.6 ± 0.6个细胞/单位面积; P <0.001）。嗜酸性粒细胞增多症扩展到区域淋巴结。TEM证实了嗜酸性粒细胞的上皮下和血管周围定位。大气道上皮中的粘液细胞从1.5 ± 0.8（OVA/SAL小鼠）增加到OVA/OVA处理的小鼠中的39.5 ± 5.7个细胞/mm BM（P <0.001）。OVA/SAL小鼠与其他对照组无差异。野生型小鼠（每组n = 6-7）中的相应实验显示了定性相似但不太明显的嗜酸性粒细胞和粘液细胞变化。在所有OVA/OVA处理的小鼠的肺中巨噬细胞和CD 4 + T细胞增加。肥大细胞数量没有差异，但脱粒仅在OVA/OVA处理的野生型小鼠中检测到。因此，在不涉及B细胞和IG的情况下，对OVA进行免疫接种，然后进行OVA攻击，在小鼠的气道和肺中引起富含嗜酸性粒细胞的炎症。
Immunoglobulins (Ig), particularly IgE, are believed to be crucially involved in the pathogenesis of asthma and, equally, in allergic models of the disease. To validate this paradigm we examined homozygous mutant C57BL/6 mice, which are B cell deficient, lacking all Ig. Mice were immunized intraperitoneally with 10 μg ovalbumin (OVA) plus alum, followed by daily (day 14–20) 30 min exposures to OVA aerosol (OVA/OVA group). Three control groups were run: OVA intraperitoneally plus saline (SAL) aerosol (OVA/SAL group); saline intraperitoneally plus saline aerosol; saline intraperitoneally plus OVA aerosol (n = 6–7). Lung and large airway tissues obtained 24 h after the last OVA or SAL exposure were examined by light microscopy and transmission electron microscopy (TEM). The Ig-deficient mice receiving OVA/ OVA treatment had swollen and discolored lungs and exhibited marked eosinophilia both in large airway subepithelial tissue (49.2 ± 12.0 cells/mm basement membrane [BM] versus OVA/ SAL control 1.2 ± 0.3 cells/mm BM; P <0.001), and perivascularly and peribronchially in the lung (49.3 ± 9.0 cells/unit area versus OVA/SAL control 2.6 ± 0.6 cells/unit area; P <0.001). The eosinophilia extended to the regional lymph nodes. TEM confirmed the subepithelial and perivascular localization of eosinophils. Mucus cells in large airway epithelium increased from 1.5 ± 0.8 (OVA/SAL mice) to 39.5 ± 5.7 cells/mm BM in OVA/OVA treated mice (P <0.001). OVA/SAL mice never differed from the other control groups. Corresponding experiments in wild-type mice (n = 6–7 in each group) showed qualitatively similar but less pronounced eosinophil and mucus cell changes. Macrophages and CD4+ T cells increased in lungs of all OVA/OVA-treated mice. Mast cell number did not differ but degranulation was detected only in OVA/OVA-treated wild-type mice. Immunization to OVA followed by OVA challenges thus cause eosinophil-rich inflammation in airways and lungs of mice without involvement of B cells and Ig.
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DOI：
10.1084/jem.184.4.1483
发表时间：
1996-10-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
通讯作者：
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白介素5缺乏消除小鼠哮喘模型中的嗜酸性粒细胞，气道高反应性和肺损伤。
影响因子：
15.3
作者：
Foster, PS;Hogan, SP;Ramsay, AJ;Matthaei, KI;Young, IG
通讯作者：
Young, IG
DOI：
10.1164/ajrccm/146.4.900
发表时间：
1992-10-01
期刊：
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子：
--
作者：
GANT, V;CLUZEL, M;HAMBLIN, AS
通讯作者：
HAMBLIN, AS
DOI：
10.1164/ajrccm.153.2.8564094
发表时间：
1996-02-01
影响因子：
24.7
作者：
Kidney, JC;Wong, AG;Hargreave, FE
通讯作者：
Hargreave, FE
DOI：
10.1152/ajplung.1996.271.3.l476
发表时间：
1996-09-01
影响因子：
4.9
作者：
Krinzman, SJ;DeSanctis, GT;Finn, PW
通讯作者：
Finn, PW