Depleted intestinal goblet cells and severe pathological changes in SCID mice infected with Heligmosomoides polygyrus
Depleted intestinal goblet cells and severe pathological changes in SCID mice infected with Heligmosomoides polygyrus
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DOI：
10.1111/j.1365-3024.2009.01123.x
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发表时间：
2009-08-01
影响因子：
2.2
通讯作者：
Arizono, N.
中科院分区：
文献类型：
--
作者：
Hashimoto, K.;Uchikawa, R.;Arizono, N.
为了确定T细胞和肥大细胞在肠道病理和肠道线虫免疫驱逐中的作用，我们分析了T细胞和b细胞缺陷严重联合免疫缺陷（SCID）小鼠、胸腺型nu/nu小鼠和肥大细胞缺陷型W/W-v小鼠感染多回Heligmosomoides后的蠕虫负荷、杯状细胞反应和绒毛结构。与野生型对照相比，SCID和nu/nu小鼠在感染后第9周的蠕虫负荷显著增加。SCID和nu/nu小鼠显示杯状细胞增生和/或Muc 2表达受损，表明这两种事件都依赖于t细胞。另一方面，与野生型对照相比，SCID小鼠的病理（绒毛萎缩和隐窝增生）和增殖细胞核抗原阳性细胞的数量增加。相反，W/W-v小鼠能够正常排出蠕虫，具有正常的杯状细胞增生，并且没有显示出在SCID小鼠中看到的粘膜结构变化，证实这些变化并不一定需要正常的肥大细胞反应。这些结果表明，功能性t细胞反应，而不是肥大细胞反应，是抗寄生虫反应、杯状细胞功能和维持正常粘膜结构所必需的。
P>To determine the role of T cells and mast cells in intestinal pathology and immune expulsion of intestinal nematodes, worm burdens, goblet cell responses and villus structures were analysed in T- and B-cell-deficient severe combined immunodeficiency (SCID) mice, athymic nu/nu mice and mast cell deficient W/W-v mice after infection with the nematode Heligmosomoides polygyrus. SCID and nu/nu mice showed significantly higher worm burdens at week 9 post-infection compared with the wild-type controls. SCID and nu/nu mice showed compromised goblet cell hyperplasia and/or Muc 2 expression, indicating that both events are T-cell dependant. On the other hand, the SCID mice showed increased pathology (villus atrophy and crypt hyperplasia) and increased numbers of proliferating cell nuclear antigen positive cells compared to the wild-type controls. W/W-v mice, conversely, were able to expel the worms normally, had normal goblet cell hyperplasia, and did not demonstrate the changes in mucosal architecture seen in SCID mice, confirming that a normal mast cell response is not necessarily required for these changes. These results suggest that a functional T-cell response, but not a mast cell response, is necessary for anti-parasite responses, goblet cell function, and maintaining normal mucosal architecture.