Establishment of mice pneumonia model with imipenem-resistant Acinetobacter baumannii
10.3760/cma.j.issn.1009-9158.2010.08.015
- VernacularTitle:亚胺培南耐药鲍曼不动杆菌小鼠肺部感染模型建立
- Author:
Daojun YU
;
Yunsong YU
;
Xiang FANG
;
Xianjun WANG
;
Yijian PAN
- Publication Type:Journal Article
- Keywords:
Acinetobacter baumannii;
Acinetobacter infections;
Pneumonia,bacterial;
Disease models,animal;
Imipenem
- From:
Chinese Journal of Laboratory Medicine
2010;33(8):771-775
- CountryChina
- Language:Chinese
-
Abstract:
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.
