Cellular localization of tumor necrosis factor (TNF)-alpha transcripts in normal bowel and in necrotizing enterocolitis. TNF gene expression by Paneth cells, intestinal eosinophils, and macrophages.
Cellular localization of tumor necrosis factor (TNF)-alpha transcripts in normal bowel and in necrotizing enterocolitis. TNF gene expression by Paneth cells, intestinal eosinophils, and macrophages.
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发表时间：
1993-06
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通讯作者：
X. Tan;W. Hsueh;F. Gonzalez‐Crussi
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作者：
X. Tan;W. Hsueh;F. Gonzalez‐Crussi
肿瘤坏死因子-α (TNF) 已被证明可诱导动物肠坏死。此外，坏死性小肠结肠炎患者的血浆 TNF 水平升高。因此，TNF可能在NEC的发病机制中发挥作用。在本研究中，我们使用原位杂交（使用人 TNF 核糖核酸探针）来定位正常活检和 NEC 患者肠道组织中的 TNF 转录本。我们发现在正常肠道中，少量的TNF mRNA仅存在于潘氏细胞中。相反，在 NEC 急性期，在潘氏细胞以及浸润性嗜酸性粒细胞中检测到大量 TNF 转录物。在一例显示巨噬细胞浸润的病例中，在这些细胞中也检测到了 TNF mRNA。固有层中的巨噬细胞和其他炎症细胞的 TNF 转录物呈阴性。我们的结果表明：1) 潘氏细胞是正常肠道中 TNF 转录物的主要来源，2) 潘氏细胞以及 NEC 患者的浸润性嗜酸性粒细胞和巨噬细胞中 TNF mRNA 的形成显着增加。含有 TNF 的细胞可能在 NEC 的病理生理学中发挥重要作用。
Tumor necrosis factor-alpha (TNF) has been shown to induce intestinal necrosis in animals. Moreover, plasma TNF levels are elevated in patients with necrotizing enterocolitis. Thus, it is possible that TNF plays a role in the pathogenesis of NEC. In the present study we used in situ hybridization (with human TNF riboprobes) to localize TNF transcripts in the intestinal tissues from normal biopsies and NEC patients. We found that in normal intestine a small amount of TNF mRNA was present only in Paneth cells. In contrast, in the acute stage of NEC, a high amount of TNF transcripts was detected in Paneth cells as well as in infiltrating eosinophils. In one case that showed infiltrating macrophages, TNF mRNA was also detected in these cells. Resident macrophages in the lamina propria and other inflammatory cells were negative for TNF transcripts. Our results suggest that: 1) Paneth cells are the major source of TNF transcripts in normal intestine, and 2) there is a marked increase in TNF mRNA formation in Paneth cells, as well as in infiltrating eosinophils and macrophages in patients with NEC. TNF-containing cells may play an important role in the pathophysiology of NEC.