跳到主要內容

臺灣博碩士論文加值系統

(216.73.216.17) 您好!臺灣時間:2025/09/03 09:27
字體大小: 字級放大   字級縮小   預設字形  
回查詢結果 :::

詳目顯示

我願授權國圖
: 
twitterline
研究生:王靜佩
研究生(外文):Wang, Jean-Pei
論文名稱:伏馬鐮孢毒素B1(FumonisinB1)對豬肺泡巨噬細胞與週邊血液單核細胞的毒害
論文名稱(外文):The immunotoxicity of fumonisin B1 in swine alveolar macrophage and peripheral blood mononuclear cells
指導教授:龐飛龐飛引用關係鄭謙仁---
指導教授(外文):Victor Fei PangChian-Ren Jeng
學位類別:碩士
校院名稱:國立臺灣大學
系所名稱:獸醫學系研究所
學門:獸醫學門
學類:獸醫學類
論文種類:學術論文
論文出版年:1998
畢業學年度:86
語文別:中文
論文頁數:90
中文關鍵詞:伏馬鐮孢毒素B1巨噬細胞週邊血液單核細胞
外文關鍵詞:Fumonisin B1macrophageperipheral blood mononuclear cells
相關次數:
  • 被引用被引用:2
  • 點閱點閱:725
  • 評分評分:
  • 下載下載:0
  • 收藏至我的研究室書目清單書目收藏:0
伏馬鐮孢毒素(fumonisins)是一群主要由鐮孢菌屬
(Fusarium spp.)產生,且化學結構相似的黴菌
毒素,其中以fumonisin B1(FB1)為最主要,致害
也最大。臨床上FB1的中毒已證實會引發動物致命的
疾病,如馬的腦白質部軟化症(equine
leukoencephalomalacia, ELEM)、豬的肺水腫
(porcine pulmonary edema, PPE)、大鼠的肝癌
及禽類的免疫傷害等。
本實驗目的在探討FB1 對豬隻免疫細胞可能具有
的影響,我們選擇免疫系統中的兩大重要細胞,肺泡
巨噬細胞(pulmonary alveolar macrophage, AM)
與週邊血液單核細胞(peripheral blood mononuclear
cell, PBMC),在活體外的條件下,將 AM 分別與
2、10 及 20 mg/ml 之 FB1 共同培養 6、24、48 及
72 小時;另將 PBMC 分別與 2、10 及 20 mg/ml 之
FB1 共同培養 12、24、48 及 72 小時,評估該等細胞
的 viability 與功能是否會受到影響。同時,我們另以
lipopolysaccharide(LPS)與 concanavalin A(ConA)
兩種致裂原 (mitogen),分別刺激 AM 與 PBMC,
使其成為活化狀態,藉以瞭解不同活化狀態下的細胞,
對於 FB1 的感受性是否相同。在 AM 方面,分別測其
細胞的 viability、吞菌與殺菌能力以及自由基
(Superoxide 與 hydrogen peroxide(O2- , H2O2))、
Tumor necrosis factor-a(TNF-a)與前列腺素E2
(PGE2)的產生能力。在 PBMC 方面,則測定細胞的
viability、DNA、 RNA 及 protein 的合成能力以及
IL-2 的產生能力。在 AM方面,實驗結果顯示:
1)在 viability 的測定結果中,AM 的 viability
在 FB1 攻毒後,呈現一種早期提升而晚期抑制的情形,
且這樣的趨勢,以經 LPS 活化的細胞反應得較非活化
細胞為早。2)以 FB1 攻毒後,AM 自由基(O2- 和
H2O2)的產生能力會受到抑制;FB1 處理組的細胞對於
受到Phorbol 12-myristate 13-Acetate(TPA)刺激後
所引發的 O2 - 產生能力較對照組為差,而此抑制情形
在經 LPS活化與非活化 AM 分別於 FB1 處理後 48 與
72 小時達到顯著性水準(p<0.05);至於 H2O2 產生
能力的抑制情形較 O2 - 輕微,在攻毒之後 72 小時,
處理組的 H2O2 產生能力有明顯的被抑制現象
(p<0.05)。 3)FB1 攻毒組對 Candida albicans
的吞菌能力較對照組差,且有隨攻毒時間的延長而
下降程度越大的趨勢;從攻毒 48 小時開始,LPS 活化
與非活化狀態的 AM 之吞菌能力被抑制的情形即有明顯
的差異存在,其中經 LPS 活化 AM 之 FB1 處理組的
吞菌能力受抑制的情形比非活化 AM 來得明顯。
4)以 FB1 攻毒後,AM 對 C. albicans 的殺菌能力
會受到抑制,且經 LPS 活化 AM 較明顯,而此抑制程度
與濃度成正相關,在攻毒 72 小時後,LPS活化與非活化
狀態 AM 的殺菌能力均顯著的被抑制。 5) FB1 會造成
經 LPS 活化 AM 之 TNF-a 的產生能力下降,而非活化
AM 之 TNF-a 產生能力在攻毒早期呈現抑制的趨勢,
但到了攻毒後 48 與 72 小時,則反有提高的趨勢。
6)FB1 對於經 LPS活化與非活化 AM 之 PGE2 產生
能力的影響不盡相同,活化狀態 AM 的 PGE2 產生是
呈現上昇的現象,而在非活化 AM,則是在攻毒後 6 -
24 小時,PGE2 的產生呈增加的趨勢,但在攻毒 48 -
72 小時,則呈抑制的現象。在 PBMC 方面,實驗結果
顯示: 1)以 FB1 攻毒後,PBMC 的 viability 普遍
的被抑制。 2)FB1 對於 PBMC 之 IL-2 產生能力的
影響,並不十分一致,但是大致呈現抑制的趨勢。
3)FB1 對於 DNA、RNA 及 protein 這三種大分子的
合成能力呈現抑制作用,其中以 RNA 和 protein
較為明顯,尤其是 RNA 於攻毒後 6 小時即顯著的
低於對照組;比較兩種不同活化狀態 PBMC 的反應,
在 RNA 與 protein 的抑制方面,以 ConA 活化的
PBMC 抑制現象稍較明顯,但在 DNA 合成能力方面,
則在經 LPS 活化與非活化二種狀態的細胞間無明顯
差異。由我們的實驗結果推測在活體中,FB1 的中毒
會造成豬隻免疫系統的抑制,若長期攝取受到 FB1
污染的飼料,可能會造成豬隻對於疾病抵抗力的降低。
Fumonisin is a group of structually related mycotoxins produced by Fusarium sp
ecies. Fumonisin B1(FB1), the major compound of fumonisin mycotoxins, has lo
ng been implicated as an etiological agent of many fatal diseases in the anima
l, such as equine leukoencephalomalacia(ELEM)and porcine pulmonary edema(PP
E); it is also responsible for the immunotoxic effect in poultry and hepatoca
rcinogenesis in rats. The purpose of the study was to evaluate the potential e
ffect of FB1 on swine pulmonary alveolar macrophages(AM)and peripheral blood
mononuclear cells(PBMC)。The cells were exposed in vitro to 2, 10, and 20 m
g FB1/ml for 6, 24, 48, and 72 hours in AM, and for 12, 24, 48, and 72 hours i
n PBMC. The cell viability and various functions of both cells were examined a
fter FB1 exposure. In addition, AM and PBMC were also activated by LPS and Con
A, respectively, to compare the susceptibility of resting and activated cells
to FB1 toxicity. For AM, parameters examinedincluded cell viability; phagocyto
tic and microbicidal potential; free radical(Superoxide and hydrogen peroxide
)(O2- and H2O2), TNF-a, and PGE2 production. For PBMC, cell viability; IL-2
production; DNA, RNA, and protein synthesis were examined. For AM, the result
s showed that following FB1 exposure, 1)the cell viability was elevated withi
n the first incubation day, but was decreased thereafter. The trend of cell re
sponse appeared earlier in LPS-stimulated (activated) than in resting AM; 2)T
PA-stimulated free radical production, including O2- and H2O2 ,was inhibited w
ith a significant reduction in O2- and H2O2 production after 48 and 72 hours o
f treatment, respectively, in both LPS-stimulated (activated) and resting AM;
3)the phagocytotic potential was depressed significantly after 48 hours of in
cubaton in both LPS-stimulated (activated) and resting AM with the former affe
cted more evidently; 4)microbicidal potential was reduced significantly by 72
hours in both LPS-stimulated (activated) and resting AM in a dose-dependent m
anner; 5)TNF-a production in LPS-stimulated (activated) AM was decreased thro
ugout the study while in resting AM it was reduced during the early time point
s but increased after 48 hours; 6)changes in PGE2 production were different i
n LPS-stimulated (activated) and resting AM. It was increased in activated AM
while in resting AM, it was increased before 24 hours of incubation followed b
y decreasing later on. As for the effect of FB1 on PBMC, it is revealed that 1
)the cell viability was declined throughout the study; 2)IL-2 production was
only slightly reduced; 3)the DNA, RNA, and protein synthesis were all decrea
sed with RNA and protein synthesis affected the most. Significant inhibition i
n RNA synthesis occurred 6 hours after FB1 exposure. The inhibitory effect of
FB1 on RNA and protein synthesis was more obvious in ConA-stimulated PBMC than
in resting cells, but there was no difference between the two types of PBMC i
n DNA synthesis. The results suggest that FB1 mycotoxicosis has the potential
to cause immunosuppression in swine. Thus, long-term ingestion of FB1-contamin
ated feed may result in an increased disease susceptibility in pigs.
QRCODE
 
 
 
 
 
                                                                                                                                                                                                                                                                                                                                                                                                               
第一頁 上一頁 下一頁 最後一頁 top