Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/52283
標題: 益生菌調節因感染所導致之發炎反應之研究
Modulation of infection induced inflammatory response by probiotic strains
作者: 謝佩珊
Hsieh, Pei-Shan
關鍵字: 益生菌
Probiotic
發炎
致病菌
Inflammation
pathogen
出版社: 食品暨應用生物科技學系所
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摘要: 乳酸菌一直以來在腸道的常態性菌叢中被提出研究其功能性,並且將確認具備功能性之乳酸菌株稱為益生菌,也就是食用後對人體健康是有幫助的。本研究開始時比較13株乳酸菌的能力後,使用6株菌進行更深入的研究,這六株菌在對表皮黏膜細胞的附著性、對病原菌的抑制性以及調節免疫反應的能力皆有所不同。在表皮黏膜細胞附著性試驗上使用五個不同部位,包含口腔、咽喉、胃部、腸道及陰道,因此在致病菌的部分,於口腔及咽喉代表菌株為肺炎鏈球菌,胃部則為胃幽門螺旋桿菌,腸道使用大腸桿菌以及陰道使用陰道加德納氏菌、白色念珠菌,用以對比不同組織感染的狀況。除此之外,在免疫反應研究的部分則以人體免疫的初代細胞以及表皮黏膜細胞株做為觀察標的,由病原菌及乳酸菌共同刺激後,偵測細胞激素IL-10, IL-12p70, interferon-γ, tumor necrosis factor-α, IL-5 and transforming growth factor-β以及趨化激素IL-8為研究重點。動物試驗部分則以胃部試驗及足跖腫脹試驗做為感染及發炎的模式,來探討乳酸菌對於病原菌感染排除及發炎症狀的調節,是否能夠有此功效。依據實驗的結果,每株菌對於免疫途徑的影響以及致病菌的抑制能力皆有所不同,嗜酸乳桿菌TYCA15是抑制胃幽門螺旋桿菌最強的菌株,但無免疫調節的能力;約氏乳桿菌MH-68與唾液乳桿菌AP-32抑制胃幽門螺旋桿菌的能力相當,但MH-68對於因感染所導致的發炎狀況,雖然有能力減緩發炎現象,但調節能力沒有AP-32好;格氏乳桿菌AI-88對免疫途徑的影響較偏向TH1/TH17的方向,且對於胃幽門螺旋桿菌之外的四種致病菌對細胞吸附性的排除功能及生長活性抑制能力皆相當好;鼠李糖乳桿菌CT-53對免疫途徑的影響較偏向TH2/TH1的方向,在固態抑菌試驗中,對於胃幽門螺旋桿菌之外的四種致病菌的存活抑制很顯著;嗜酸乳桿菌F-1對於免疫途徑的影響則有平衡的能力,主要是能刺激較多種免疫細胞的增生活性,且對於誘導免疫細胞分泌細胞激素的種類及產量,多數比其他菌株佳且顯著,因此推測對於TH1/TH2或TH17/Treg之間的平衡有助益,而對於致病菌株,則是除了胃幽門螺旋桿菌外,其他四株菌的抑制性,無論是在固態抑菌試驗或是致病菌對細胞吸附性的排除功能及生長活性抑制能力都十分顯著;唾液乳桿菌AP-32是本研究中唯一確認能夠調節Treg途徑的菌株,且對於因致病菌所導致的發炎現象,能夠緩解過度發炎的反應,並且對於致病菌的抑制性雖無F-1強烈,但能力也屬上乘。 由本研究之結果充分確認宿主、病原菌及益生菌之間的交互作用及關係,再者,由於益生菌之功能互有強弱之別,在菌株功能不相衝突之情況下,或許複方的益生菌配方能夠對於促進健康的功能上有加成的效果,也許能夠提供給人類有較好的健康效益。
Lactic acid bacteria are important human commensal microbiota that are considered to be probiotics as they have been shown to reduce pathogenic infections and chronic inflammation. In this study, six strains of lactobacilli were compared for their probiotic potential. These 6 strains showed varying capacities for adhesion, pathogen inhibition and cytokine induction IL(interleukin)-8 and IL-10) in different human epithelial cells, such as primary cultures of buccal cavity cells, and established cell lines derived from epithelia of the pharynx, stomach, intestine, and cervix. After exposure to lactobacilli, secretion of cytokines (IL-10, IL-12p70, interferon-γ, tumor necrosis factor-α, IL-5 and transforming growth factor-β) was induced at varying levels in different cultures of human immune cells, including dendritic cells, monocyte-depleted peripheral blood mononuclear cells, CD14+ cells, CD4+CD25- T cells, and regulatory T-cells (CD4+CD25+ T cells). Growth inhibition of pathogenic strains was detectable in the presence of lactobacilli in vitro. Using animal models, regulation of gastric acid, carrageenan-induced edema in the hind paw was studied to indicate inflammatory condition and histopathologic changes accompanying anti-H. pylori activity. Moreover, Lactobacillus acidophilus TYCA15 was found the strongest inhibition of H. pylori but no function of immunomodulation; Lactobacillus johnsonii MH-68 was found stronger inhibition of H. pylori than others and a little function of immunomodulation; Lactobacillus gasseri AI-88 was found to skew TH1/TH17 pathway and the highest inhibition of growth and adhesion of pathogen except H. pylori; Lactobacillus rhamnosus CT-53 was found to skew TH2/TH1 pathway and stronger antagonism of pathogen than others except H. pylori; Lactobacillus acidophilus F-1 was found to balance TH1/TH2 or TH17/Treg pathway, and the higher inhibition of growth and adhesion of pathogen than others except H. pylori and the strongest antagonism of pathogen except H. pylori, too. Lactobacillus salivarius sp. salicinius AP-32 was found to have the highest probiotic potential to modulate the inflammation which was induced by pathogen and the ability of inhibition activity of pathogen was better than others. This study highlights the complex host-pathogen-microbiota interactions and indicates that a combination of strains may have to be used to provide all the desirable probiotic benefits if the immunomodulation pathway was in the same way.
URI: http://hdl.handle.net/11455/52283
其他識別: U0005-2006201315445500
文章連結: http://www.airitilibrary.com/Publication/alDetailedMesh1?DocID=U0005-2006201315445500
Appears in Collections:食品暨應用生物科技學系

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