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頁籤選單縮合
題名 | 粗製巴斯德桿菌D型毒素誘發腫瘤壞死因子-α產生與豬萎縮性鼻炎關係之探討=Crude Pasteurella Multocida Type D Toxin Inducing TNF-α Production in Swine Atrophic Rhinitis |
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作者 | 李維誠; 蘇秀琪; 簡茂盛; 林正忠; 稻葉右二; 劉正義; | 書刊名 | 中華民國獸醫學會雜誌 |
卷期 | 24:3 1998.09[民87.09] |
頁次 | 頁188-195 |
分類號 | 437.657 |
關鍵詞 | 巴斯德桿菌D型毒素; 豬萎縮性鼻炎; 腫瘤壞死因子; 巨噬細胞; Pasteurella multocida type D toxin; Swine atrophy rhinitis; Tumor necrosis factor-α; Alveolar macrophage; |
語文 | 中文(Chinese) |
中文摘要 | 巴斯德桿菌 D 型毒素( P. multocida type D toxin; PMT )為引致豬萎縮性鼻 炎( atrophic rhinitis; AR )之主要致病因子,具有多樣生物活性。為探討 PMT 是否具 有誘發腫瘤壞死因子( tumor necrosis factor- α;TNF- α)產生之生物活性和 TNF- α 在 AR 中可能扮演之角色,吾等以粗製 PMT 和經陰離子交換層析法半純化之 PMT, 刺激豬 肺泡巨噬細胞( alveolar macrophage;AM ),然後檢測細胞培養上清液中 TNF- α之濃度 和生物活性。 結果顯示粗製 PMT 及半純化 PMT 刺激 AM 之上清液對 PK-15 的毒殺能力及 TNF- α濃度,隨 PMT 對 AM 培養時間的增長而增加, 並有明顯之劑量效應,在攻毒後 24 小時對 PK-15 之毒殺能力最高。 為進一步暸解鼻腔黏膜中 TNF- α在 AR 中可能扮演之相 關角色,從屠宰場收集豬隻之鼻腔黏膜組織, 經均質化後以 ELISA 法檢測組織中 TNF- α 濃度,在鼻甲骨外觀正常或輕微病變之檢體,其鼻甲骨黏膜中之 TNF- α濃度極顯著低於鼻 甲骨明顯嚴動萎縮之檢體( P<0.01 )。 由上述實驗得知, 粗製 PMT 及半純化 PMT 具有 引發 AM 產生 TNF- α的能力,其在 AR 的致病機制中與 AR 病變形成有關。 |
英文摘要 | Pasteurella multocida type D toxin (PMT) is the major factor in the pathogenesis of swine atrophy rhinitis (AR). To investigate the characteristics of the PMT, tumor necrosis factor-α (TNF-α) biological activity and concentration in cultural supernatants released from crude and partially purified PMT-stimulating alveolar macrophages (AM) were examined by cytotoxic assay to PK-15 cell line and ELISA respectively. The result showed the dose-dependent and time-related cytotoxicity of cultured supernatants of PMT-stimulating AM to PK-15 cells. The maximal cytotoxic activity to PK-15 cells was found in the cultured supernatant of AM with 24-hour-stimulation by crude and partially purified PMT. To study the relationship between TNF-α levels and turbinate lesion, the turbinate mucosa of pigs with or without AR lesion were collected from slaughter house and the amounts of TNF-α in tissues were determined by ELISA assay. The results showed that the levels of TNF-α in pigs with severe AR were significantly higher than those with no or mild turbinate lesions (p<0.01). These results suggested that PMT could induce macrophages releasing TNF-α in turbinate mucosa that might contribute the pathogenesis of AR. |
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