中华检验医学杂志
中華檢驗醫學雜誌
중화검험의학잡지
CHINESE JOURNAL OF LABORATORY MEDICINE
2010年
8期
771-775
,共5页
余道军%俞云松%方翔%王贤军%潘熠健
餘道軍%俞雲鬆%方翔%王賢軍%潘熠健
여도군%유운송%방상%왕현군%반습건
鲍氏不动杆菌%不动杆菌感染%肺炎,细菌性%疾病模型%动物%亚胺培南
鮑氏不動桿菌%不動桿菌感染%肺炎,細菌性%疾病模型%動物%亞胺培南
포씨불동간균%불동간균감염%폐염,세균성%질병모형%동물%아알배남
Acinetobacter baumannii%Acinetobacter infections%Pneumonia,bacterial%Disease models,animal%Imipenem
目的 建立亚胺培南耐药鲍曼不动杆菌小鼠肺部模型,为泛耐药鲍曼不动杆菌抗感染研究提供实验动物模型.方法 随机选取120只约4周大雄性BALB/C小鼠,平均分成3组:微量气管注射法组、超声雾化法组和滴鼻法组.每组小鼠用甲氨蝶呤化疗降低BALB/C小鼠的免疫力,然后将亚胺培南耐药鲍曼不动杆菌分别用微量气管注射法、超声雾化法、滴鼻法感染免疫力低下和正常的BALB/C小鼠,检测微量气管注射法、超声雾化法、滴鼻法感染的小鼠感染率、死亡率、细菌清除率、肺部病理变化.结果 微量气管注射法、超声雾化法感染免疫力低下的BALB/C小鼠的肺部感染率均为100%(30/30),死亡率分别为100%(10/10),33%(3/10),2组小鼠肺部细菌感染12~24 h后支气管周及肺泡间质内见中性粒细胞、淋巴细胞、巨噬细胞为主的炎症细胞浸润,微量气管注射法感染的小鼠部分肺泡组织结构崩解,肺泡腔内可见脓肿形成及较多细菌集落,超声雾化法感染的小鼠24 h见肺部部分区域存在细胞变性,但支气管及肺泡组织结构基本正常,肺泡壁血管轻度扩张伴淤血,24~48 h后可见支气管和支气管周围变性,部分肺组织血管高度扩张,伴有水肿,48 h后炎症逐渐恢复.滴鼻法感染免疫力低下的BALB/C小鼠的肺部感染不明显,未见小鼠死亡(0/10),肺部无明显病理变化.结论 免疫力低下BALB/C小鼠可以通过微量气管注射法和超声雾化法建立亚胺培南耐药鲍曼不动杆菌肺部感染模型,超声雾化法可以大批量同时操作,简单经济快速,实用性强.亚胺培南耐药鲍曼不动杆菌难以感染免疫力正常小鼠.
目的 建立亞胺培南耐藥鮑曼不動桿菌小鼠肺部模型,為汎耐藥鮑曼不動桿菌抗感染研究提供實驗動物模型.方法 隨機選取120隻約4週大雄性BALB/C小鼠,平均分成3組:微量氣管註射法組、超聲霧化法組和滴鼻法組.每組小鼠用甲氨蝶呤化療降低BALB/C小鼠的免疫力,然後將亞胺培南耐藥鮑曼不動桿菌分彆用微量氣管註射法、超聲霧化法、滴鼻法感染免疫力低下和正常的BALB/C小鼠,檢測微量氣管註射法、超聲霧化法、滴鼻法感染的小鼠感染率、死亡率、細菌清除率、肺部病理變化.結果 微量氣管註射法、超聲霧化法感染免疫力低下的BALB/C小鼠的肺部感染率均為100%(30/30),死亡率分彆為100%(10/10),33%(3/10),2組小鼠肺部細菌感染12~24 h後支氣管週及肺泡間質內見中性粒細胞、淋巴細胞、巨噬細胞為主的炎癥細胞浸潤,微量氣管註射法感染的小鼠部分肺泡組織結構崩解,肺泡腔內可見膿腫形成及較多細菌集落,超聲霧化法感染的小鼠24 h見肺部部分區域存在細胞變性,但支氣管及肺泡組織結構基本正常,肺泡壁血管輕度擴張伴淤血,24~48 h後可見支氣管和支氣管週圍變性,部分肺組織血管高度擴張,伴有水腫,48 h後炎癥逐漸恢複.滴鼻法感染免疫力低下的BALB/C小鼠的肺部感染不明顯,未見小鼠死亡(0/10),肺部無明顯病理變化.結論 免疫力低下BALB/C小鼠可以通過微量氣管註射法和超聲霧化法建立亞胺培南耐藥鮑曼不動桿菌肺部感染模型,超聲霧化法可以大批量同時操作,簡單經濟快速,實用性彊.亞胺培南耐藥鮑曼不動桿菌難以感染免疫力正常小鼠.
목적 건립아알배남내약포만불동간균소서폐부모형,위범내약포만불동간균항감염연구제공실험동물모형.방법 수궤선취120지약4주대웅성BALB/C소서,평균분성3조:미량기관주사법조、초성무화법조화적비법조.매조소서용갑안접령화료강저BALB/C소서적면역력,연후장아알배남내약포만불동간균분별용미량기관주사법、초성무화법、적비법감염면역력저하화정상적BALB/C소서,검측미량기관주사법、초성무화법、적비법감염적소서감염솔、사망솔、세균청제솔、폐부병리변화.결과 미량기관주사법、초성무화법감염면역력저하적BALB/C소서적폐부감염솔균위100%(30/30),사망솔분별위100%(10/10),33%(3/10),2조소서폐부세균감염12~24 h후지기관주급폐포간질내견중성립세포、림파세포、거서세포위주적염증세포침윤,미량기관주사법감염적소서부분폐포조직결구붕해,폐포강내가견농종형성급교다세균집락,초성무화법감염적소서24 h견폐부부분구역존재세포변성,단지기관급폐포조직결구기본정상,폐포벽혈관경도확장반어혈,24~48 h후가견지기관화지기관주위변성,부분폐조직혈관고도확장,반유수종,48 h후염증축점회복.적비법감염면역력저하적BALB/C소서적폐부감염불명현,미견소서사망(0/10),폐부무명현병리변화.결론 면역력저하BALB/C소서가이통과미량기관주사법화초성무화법건립아알배남내약포만불동간균폐부감염모형,초성무화법가이대비량동시조작,간단경제쾌속,실용성강.아알배남내약포만불동간균난이감염면역력정상소서.
Objective To construct the mice pneumonia model with imipenem-resistant Acinetobacter baumannii and provide experimental model in anti-pan-resistant Acinetobacter baumannii therapy study. Methods A total number of 120 4-week-old BALB/C male mice were randomly selected and divided into three groups including micro-intratracheal injection, ultrasonic atomizing and nasal dripping. The mice were treated with methotrexate to induce hypo-immunity in every group. These BALB/C mice of normal immunity and hypo-immunity were infected through Imipenem-resistant Acinetobacter baumannii by microintratracheal injection, ultrasonic atomizing and nasal dripping, respectively. The morbidity, mortality,bacterial clearance rate and histopathology in lung were determined. Results The morbidities of BALB/C mice with hypo-immunity infected by micro-intratracheal injection and ultrasonic atomizing achieved 100%(30/30), while the mortalities were 100% (10/10) and 33.3% (3/10), respectively. Mice in two groups above displayed the influx of neutrophils, lymphocytes and macrophages in the peri-bronchial and alveolar interstitial space 12-24 h after pulmonary infection. In addtion, the mice in micro-intratracheal injection group displayed coUapse of partial alveolar walls, formation of abscesses and bacterial colonies in alveoli. While the lung pathology in mice of ultrasonic atomizing group was characterized by cell degeneration in some regions in the lungs, slight relaxation, congestion in alveolar wall vessels and normal of bronchial and alveolar tissue 24 h after inoculation. Degeneration in peri-tracheal and peri-bronchial areas was observed 24-48 h after inoculation, along with highly expanded pulmonary blood vessels and edems. The inflammation was reduced at 48 hours. There was no obvious pulmonary infection in BALB/C mice with hypo-immunity by nasal dripping with mortality of 0% (0/10) and no significant histopathologic change in lungs. Conclusions BALB/C mice with hypo-immunity pneumonia model with Imipenem-resistant Acinetobacter baumannii can be conducted by micro-intratracheal injection or ultrasonic atomizing, but the latter has the advantages of high-productivity, easy-operation, low-cost, time-saving and usefulness. Mice with normal immunity are not susceptible to imipenem-resistant Acinetobacter baumannii.