中华微生物学和免疫学杂志
中華微生物學和免疫學雜誌
중화미생물학화면역학잡지
CHINESE JOURNAL OF MICROBIOLOGY AND IMMUNOLOGY
2011年
5期
406-412
,共7页
黄韧%邓少嫦%王颖彦%张钰%吴玉娥%李文德%赵维波%刘香梅%郭震
黃韌%鄧少嫦%王穎彥%張鈺%吳玉娥%李文德%趙維波%劉香梅%郭震
황인%산소항%왕영언%장옥%오옥아%리문덕%조유파%류향매%곽진
禽流感HSN1亚型病毒%BALB/c小鼠%T淋巴细胞%细胞因子
禽流感HSN1亞型病毒%BALB/c小鼠%T淋巴細胞%細胞因子
금류감HSN1아형병독%BALB/c소서%T림파세포%세포인자
Avian influenza A(H5N1) viruses%BALB/c mouse%T lymphocytes%Cytokine
目的 研究禽流感H5N1病毒感染BALB/c小鼠后对宿主细胞免疫功能和细胞因子水平变化的影响,探讨禽流感H5N1病毒感染哺乳动物的免疫发病机制.方法 选用鹅源禽流感H5N1病毒感染BALB/c小鼠,采用流式细胞仪检测血液和脾脏T淋巴细胞及其亚群的变化,采用ELISA检测血液中细胞岗子(IFN-γ、TNF-α、IL-4、IL-18、IL-10、IL-2)及禽流感H5N1病毒特异性抗体的变化.结果 禽流感H5N1病毒感染可引起对宿主短暂的、可恢复的细胞免疫功能损伤:血液CD3+、CD4+、CD8+ T淋巴细胞数量于染毒后第2~4天下降(第4天为最低值),脾脏T淋巴细胞数最于染毒后第5~8天下降(第6天为最低值),然后均逐渐恢复到正常水平.染毒后血液细胞因子变化表现为:血清IFN-γ、TNF-α水平下降,IL-4、IL-18、IL-10水平上升,IL-2水平无明显变化.从感染第7天开始检测H5N1禽流感特异性抗体为阳性,抗体水平逐渐升高至实验结束的感染第14天.结论 H5N1禽流感病毒感染可引起宿主T细胞免疫功能低下是其主要的免疫病理改变之一,细胞因子表达失平衡或过多的表达都可能对宿主产生免疫病理损伤.
目的 研究禽流感H5N1病毒感染BALB/c小鼠後對宿主細胞免疫功能和細胞因子水平變化的影響,探討禽流感H5N1病毒感染哺乳動物的免疫髮病機製.方法 選用鵝源禽流感H5N1病毒感染BALB/c小鼠,採用流式細胞儀檢測血液和脾髒T淋巴細胞及其亞群的變化,採用ELISA檢測血液中細胞崗子(IFN-γ、TNF-α、IL-4、IL-18、IL-10、IL-2)及禽流感H5N1病毒特異性抗體的變化.結果 禽流感H5N1病毒感染可引起對宿主短暫的、可恢複的細胞免疫功能損傷:血液CD3+、CD4+、CD8+ T淋巴細胞數量于染毒後第2~4天下降(第4天為最低值),脾髒T淋巴細胞數最于染毒後第5~8天下降(第6天為最低值),然後均逐漸恢複到正常水平.染毒後血液細胞因子變化錶現為:血清IFN-γ、TNF-α水平下降,IL-4、IL-18、IL-10水平上升,IL-2水平無明顯變化.從感染第7天開始檢測H5N1禽流感特異性抗體為暘性,抗體水平逐漸升高至實驗結束的感染第14天.結論 H5N1禽流感病毒感染可引起宿主T細胞免疫功能低下是其主要的免疫病理改變之一,細胞因子錶達失平衡或過多的錶達都可能對宿主產生免疫病理損傷.
목적 연구금류감H5N1병독감염BALB/c소서후대숙주세포면역공능화세포인자수평변화적영향,탐토금류감H5N1병독감염포유동물적면역발병궤제.방법 선용아원금류감H5N1병독감염BALB/c소서,채용류식세포의검측혈액화비장T림파세포급기아군적변화,채용ELISA검측혈액중세포강자(IFN-γ、TNF-α、IL-4、IL-18、IL-10、IL-2)급금류감H5N1병독특이성항체적변화.결과 금류감H5N1병독감염가인기대숙주단잠적、가회복적세포면역공능손상:혈액CD3+、CD4+、CD8+ T림파세포수량우염독후제2~4천하강(제4천위최저치),비장T림파세포수최우염독후제5~8천하강(제6천위최저치),연후균축점회복도정상수평.염독후혈액세포인자변화표현위:혈청IFN-γ、TNF-α수평하강,IL-4、IL-18、IL-10수평상승,IL-2수평무명현변화.종감염제7천개시검측H5N1금류감특이성항체위양성,항체수평축점승고지실험결속적감염제14천.결론 H5N1금류감병독감염가인기숙주T세포면역공능저하시기주요적면역병리개변지일,세포인자표체실평형혹과다적표체도가능대숙주산생면역병리손상.
Objective To study the cell immunity and eytokines responses to avian influenza A H5N1 virus infections in a BALB/c model to better understand the pathogenesis of H5N1 avian influenza disease. Methods Two hundred and twenty BALB/c mice of the infected group were inoculated with 0.1 ml (10-4.875 TCID50) of A/Goose/Guangdong/NH/2003 ( H5N1 ) virus intra-nasally. Fifty control mice received noninfectious allantoic fluid and another fifty control mice received normal sodium. Blood and spleen samples were collected from the live mice every 24 h during the 14 d post-infection. The changes of CD3 + T cells , CD4 + T cells, CD8 + T cells for cell immunity in blood circulation and spleen were detected by flow cytometry. And the cytokines and antibody responses in blood circulation were detected by ELISA. Necropsy was performed on mice that died during the experiment and those euthanized at end of study. Results Avian influenza A( H5N1) virus infections can make damages to the cell immune system transiently. The CD3 + T cells, CD4 + T cells, CDS + T cells declined at 24 days post infection in blood circulation and declined at 5-8 days in spleen, then recovered to the normal level gradually. The eytokines responses to the infections can be detected: the level of IFN-γ,TNF-α declined, IL-4, IL-18, IL-10 increased, and IL-2 changed little. The antibody increased rapidly from day 7 post infection until the end of the study (day 14 post infection). Conclusion Collectively, avian influenza A(H5N1) virus can cause cell immunity deficiency and an imbalance in the level of eytokines, which may contribute to the unusual severity of disease caused by the H5N1 avian influenza virus.