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1.
Chinese Journal of Digestion ; (12): 734-738, 2011.
Article in Chinese | WPRIM | ID: wpr-428192

ABSTRACT

ObjectiveTo obtain stable animal models and observe Helicobacter hepaticas (Hh)colonization and pathological claracteristics,through infecting different mice strains with Hh.Methods SPF-class male BABL/c Cr,SCID/Cr and C57BL/6 Cr mice were inoculated 0.2 ml Hh standard strain ATCC51450 bacterial suspension (1 × 108CUF/ml),inoculated for 3 times with 48 hours intervals,the control group was fed with the same volume of PBS.Mice were executed at 4 weeks,8weeks and 16 weeks since last Hh inoculation,and mice esophagus,stomach,jejunum,ileum,cecum,colon,liver and pancreas tissue were taken for histopathology examination,Micro-aerobic bacteria isolation,culture and identification and Hh specific 16S rRNA gene amplification.Results The colonization rates of Hh in cecum after inoculated in BALB/c Cr mice and SCID/Cr mice at 4 weeks,8 weeks and 16 weeks were all 8/8,colonization rates in colon at 4 weeks,8 weeks and 16 weeks were 4/8,5/8,5/8 and 3/8,6/8,5/8 respectively,colonization rates in ileum and jejunum at 16 weeks were 1/8,colonization rates in liver at 8 weeks and 16 weeks were 2/8,3/8 and 2/8,2/8respectively.The colonization rates of Hh in cecum after inoculated in C57BL/6 Cr mice at 4 weeks,8weeks and 16 weeks were 1/8,2/8 and 2/8 respectively,colonization rates in colon at 8 weeks and 16weeks were 1/8,2/8 respectively.Compared with C57BL/6 Cr mice,the inflammatory changes in liver,cecum and colon were more significant in Hh infected BALB/c Cr and SCID/Cr mice (P<0.01),and histological scores gradually increased as infection time extended (P<0.05,P< 0.01 ).The histological scores were significantly higher in those with colon and liver Hh bacterial colonization than those without Hh bacterial colonization (P<0.05).The histopathological score of cecal tissue was positively correlated with the density of Hh colonization.ConclusionDifferent mice strains are with different susceptibility to Hh,and better Hh infection model can be obtained in Hh inoculated BALB/c Cr and SCID/Cr mice.

2.
Chinese Journal of Digestion ; (12): 757-760, 2011.
Article in Chinese | WPRIM | ID: wpr-428191

ABSTRACT

Objective To establish Helicobacter pylori (Hp) infection induced chronic obstructive pulmonary disease (COPD) rat model,and to explore the role of Hp in the pathogenesis of COPD.Methods40 Wistar rats were randomly divided into double modeling group (Hp infection,smoked and intratracheal instillation of lipopolysaccharide),COPD group (smoked and intratracheal instillation of lipopolysaccharide),Hp infected group and control group.The lung function,cytokines level in serum and bronchial alveolar lavage fluid (BALF),Hp related genes expression in bronchial and lung tissue were detected.And Hp in bronchial and lung tissue was isolated and cultured.Results The lung tissue of both COPD group and double modeling group accorded with COPD pathological characteristics,and the latter was more apparent.The lung function of COPD group and double modeling group decreased more significantly than that of control group and Hp infected group (all P<0.05),and which was more obvious in double modeling group than that of COPD group (P<0.05).Along with the Hp colonization density increased,Ri and Re value of double modeling group increased (r=0.785 and 0.905),the value of Gdyn,PEF and FEV0.3/FVC decreased (r=-0.975,-0.959and -0.976).Compared with control group,IL-6,IL-8 and TNF-a cytokines levels in serum and bronchoalveolar lavage fluid of other groups increased significantly (all P<0.05),and within the groups,double modeling group increased most significantly (all P<0.05).Hp UreC gene was only amplified in part of bronchi and lung tissue of double modeling group,no Hp and suspicious bacteria colonies were isolated and cultured.ConclusionsHp not directly colonized in bronchi and lung tissue,which aggravated inflammation through increasing the serum and bronchoalveolar cytokines level of COPD rat model.Which caused the deterioration in lung function of COPD group.

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