Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/14194
標題: 放線桿菌胸膜肺炎多形態細胞形成之系列變化
Serial changes of the polymorphic cell in Actinobacillus pleuropneumonia
作者: 葛潤儀
Ko, Jun-I
關鍵字: Actinobacillus pleuropneumoniae
放線桿菌胸膜肺炎
polymorphic cell
serial changes
多形態細胞
系列變化
出版社: 獸醫學系
摘要: 中 文 摘 要 豬放線桿菌胸膜肺炎在豬隻的肺臟常可見到肺泡腔內出現大量排列成漩渦狀的多形態細胞,為瞭解這些多形態細胞之形成過程,本實驗以總菌量為5×105CFU之胸膜肺炎放線桿菌接種無特殊病原豬隻後,觀察接種細菌後第12及24小時,豬肺泡腔內細胞形態之變化,並使用穿透式電子顯微鏡觀察這些細胞之超顯微結構鑑定這些在光學顯微鏡下無法歸類的多形態細胞,以瞭解其來源及形成方式。 實驗結果顯示,接種胸膜肺炎放線桿菌出現於肺泡腔內之細胞形態是以多形態單核細胞之聚集為主。此外,在感染胸膜肺炎放線桿菌之初期,出現在肺組織及肺泡腔內的炎症細胞是以嗜中性球為主,但感染24小時以後,多形態單核細胞便成為本病最顯著的細胞形態。以穿透式電子顯微鏡觀察這些多形態單核細胞的結果顯示,雖然有些細胞瀕臨壞死,其細胞質內胞器消失,但其餘的細胞仍可依其細胞質內的特徵性胞器加以鑑別,在可鑑別的細胞中,大部份具有單核球與巨噬細胞的特徵性胞器-溶素體,小部份為具有第二型肺泡上皮細胞的特徵性胞器-板狀小體。以上結果推論,豬放線桿菌胸膜肺炎的特徵性病變多形態細胞的來源可能不只一種,單核球、巨噬細胞及第二型肺泡上皮細胞均有可能。 多形態細胞形成的方式可分為兩種,一種為血管內皮細胞受到傷害後,在血管內已變性的單核球因血管破裂流入肺泡腔中逐漸變形而成的或大量的單核球移行出血管進入肺泡腔中變形而成的;另一種則為肺泡腔中的巨噬細胞與大量增生的第二型肺泡上皮細胞受到傷害後逐漸變形而成,而細胞變形的方式在電子顯微鏡下觀察的結果顯示可能為核外被小池擴張或細胞質內的粒線體與內質網擴張或整個細胞質擴張將核擠壓變形的結果。
Abstract The polymorphic cells, arranged in swirling pattern, are usually in the pneumonic lesion of Actinobacillus pleuropneumoniae (App)-infected pig. Specific pathogen free pigs were inoculated intratracheally with App. at a concentration of 5×105 CFU, in order to understand the origin and formation processes of polymorphic cells. The pigs either died spontaneously, or were sacrificed at 12th and 24th hour after inoculation. The cells in alveolar spaces were observed with light and electron microscopes. The results indicated that in the early stage after App. inoculation, a lot of neutrophils were observed in alveolar spaces. Twenty-four hours later, polymorphic cell appeared abundantly. Although most cells were necrotic and their organelles disappeared, some cells still could be identified. Ultrastructural findings indicated that some were monocytes and macrophages, in which lysosomes were observed, and others were type Ⅱ pneumocytes, in which, lamellar bodies were observed. Two formation processes of polymorphic cells were observed. One was that monocytes migrated to alveolar spaces after endothelial cells were damaged or ruptured. The other was that alveolar macrophages and type Ⅱ pneumocytes gradually deformed after injured by App. The mechanisms of deformation were nuclear envelope blebbing, mitochondria swelling, rough endoplasmic reticulum dilatation, and cytoplasmic swelling to squeeze the nucleus. Conclusively, the appearance of polymorphic cells was relatively specific lesion of Actinobacillus pleuropneumonia. It was verified that these cells were derived from monocytes, macrophages and type Ⅱ pneumocytes.
URI: http://hdl.handle.net/11455/14194
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