【摘要】：前言 無(wú)論是以個(gè)體或組織成分存在的細(xì)胞,均對(duì)其環(huán)境的信號(hào)做出反應(yīng),并由此建立細(xì)胞間的信息傳遞。在維持組織穩(wěn)態(tài)和防御感染或非感染性損傷的宿主反應(yīng)中,細(xì)胞以自分泌或旁分泌方式借助于低分子量多肽-細(xì)胞因子調(diào)節(jié)其生長(zhǎng)和增殖。感染是病原體與宿主間相互作用的結(jié)果。研究表明,感染引起的全身性炎癥反應(yīng)綜合征(SIRS)和器官損傷中,病原體或其產(chǎn)物可能僅是觸發(fā)或始動(dòng)因素,而機(jī)體對(duì)致炎因素的應(yīng)答可能更為重要。人們首先注意到,感染性疾病時(shí)宿主應(yīng)答的一個(gè)重要方式是通過(guò)釋放前炎性細(xì)胞因子,產(chǎn)生有利或不利于感染控制的效應(yīng);而近年來(lái)也開(kāi)始注意到病原體可能利用或逃避宿主產(chǎn)生的細(xì)胞因子,并做了初步研究。在TNF-α、IL-1β和IL-6與感染性疾病的研究中發(fā)現(xiàn),這些細(xì)胞因子適量分泌有利于控制感染,過(guò)度產(chǎn)生則對(duì)機(jī)體不利;它們的濃度與疾病的嚴(yán)重程度和預(yù)后相關(guān);細(xì)胞因子持續(xù)升高者更易發(fā)生院內(nèi)感染。關(guān)于病原體可能利用或逃避宿主免疫防御的研究中,有些學(xué)者已發(fā)現(xiàn)某些細(xì)胞因子能促進(jìn)某些細(xì)菌生長(zhǎng),但相關(guān)機(jī)理不清楚,很多問(wèn)題有待研究。本實(shí)驗(yàn)選擇了與炎癥關(guān)系最為密切的細(xì)胞因子-TNF-α、IL-1β和IL-6,研究其對(duì)院內(nèi)感染中最常見(jiàn)的病原菌-綠膿桿菌、金黃色葡萄球菌和不動(dòng)桿菌體外生長(zhǎng)的影響,探討細(xì)菌和宿主細(xì)胞因子之間的相互作用,為遷延性炎癥中細(xì)菌增殖的機(jī)制提供新的依據(jù),也為評(píng)價(jià)旨在防止宿主防御反應(yīng)失調(diào)時(shí)細(xì)胞因子紊亂為切入點(diǎn)的治療手段提供進(jìn)一步的實(shí)驗(yàn)室證據(jù)。 實(shí)驗(yàn)材料和方法 一、實(shí)驗(yàn)材料
[Abstract]:Both individual and tissue components respond to signals from their environment and establish intercellular information transmission. In maintaining tissue homeostasis and host response against infection or non-infectious injury, cells autocrine or paracrine regulate their growth and proliferation by means of low molecular weight polypeptide cytokines. Infection is the result of the interaction between pathogen and host. Studies have shown that pathogens or their products may be only triggers or initiators in (SIRS) and organ damage caused by infection, but the response of organism to inflammatory factors may be more important. It is first noted that an important way of host response in infectious diseases is to produce beneficial or unfavorable effects on infection control by releasing preinflammatory cytokines. In recent years, we have also noticed that pathogens may use or escape the cytokines produced by the host, and have made a preliminary study. In the study of TNF- 偽 IL-1 尾, IL-6 and infectious diseases, it was found that the proper secretion of these cytokines was beneficial to control infection, but excessive production was harmful to the body, their concentration was related to the severity and prognosis of the disease. Increased cytokines are more likely to cause nosocomial infection. Some researchers have found that some cytokines can promote the growth of some bacteria, but the related mechanism is not clear, and many problems need to be studied. In this study, cytokines TNF- 偽, IL-1 尾 and IL-6, which are most closely related to inflammation, were selected to study the effects of TNF- 偽 IL-1 尾 and IL-6 on the growth of Pseudomonas aeruginosa, Staphylococcus aureus and Acinetobacter Acinetobacter, the most common pathogens of nosocomial infection, in vitro. The study of the interaction between bacteria and host cytokines provides a new basis for the mechanism of bacterial proliferation in persistent inflammation. It also provides further laboratory evidence for the evaluation of therapeutic approaches aimed at preventing cytokine disorders in host defense response disorders. Experimental materials and methods
【學(xué)位授予單位】：中國(guó)醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2005
【分類號(hào)】：R392

【引證文獻(xiàn)】

相關(guān)碩士學(xué)位論文 前1條

1 楊磊;奶牛乳腺炎乳汁三種細(xì)胞因子檢測(cè)及TNF-α對(duì)乳腺細(xì)胞凋亡和增殖的影響[D];內(nèi)蒙古農(nóng)業(yè)大學(xué);2010年

，

本文編號(hào)：2184280