ABSTRACT
Objective To investigate the role of CXC chemokine ligand 5 (CXCL5) in the patho-genesis of dextran sulfate sodium (DSS)-induced inflammatory bowel disease (IBD). Methods A mouse model of IBD was established by giving 3% DSS in drinking water. Influences of CXCL5 knockout on mouse body weight, clinical symptoms, survival rate, pathological injury and the secretion of inflammatory cyto-kines were analyzed. Results CXCL5 levels in serum of mice with DSS-induced IBD were significantly higher than those of the normal control group. DSS-induced weight gain, death, pathological damages and inflammatory cytokine secretion were alleviated in mice after knocking out CXCL5. Conclusion CXCL5 might promote the secretion of inflammatory cytokines in mice with DSS-induced acute colitis and aggravate pathological damages,suggesting that CXCL5 might be a potentially important candidate target for the treat-ment of IBD.
ABSTRACT
Objective To establish a non-traumatic mouse model of acid aspiration-induced lung injury which al-lows longitudinal studies.Method C57BL/6 mice were anesthetized and orotracheally intubated with a 20 gauge angio-catheter guided by optical fiber.The mice were subsequently placed in the right lateral decubitus position and external com-pression to the left lung was manually applied.A polyethylene catheter was advanced into the right lung and used to instill either hydrochloric acid (2.5μL/g, 0.1 mol/L, pH 1.5) or saline as control.Then the mice were recovered with supple-mental oxygen for 4 hours.The pulmonary physiological function and survival of mice within 2 weeks after surgery were as-sessed.Results Methylene blue instillation showed that the staining fluid went into the right lung of the non-traumatically intubated mice.The survival rate of the mice with non-traumatic instillation was 80%, statistically significantly higher than those with tracheostomy instillation.Histological examination and lung function ( wet/dry ratio, elastance and arterial oxy-gen saturation) assay demonstrated that acid instillation caused a profound pathological changes and functional impairment of the lung.Besides, acid aspiration into the mouse lung caused a significant increase in neutrophil infiltration in mouse pulmonary alveoli and high concentrations of inflammatory factors (TNF-α, IL-6, CXCL1 and CXCL2) in the bronchoalve-olar lavage fluid.Conclusions We successfully established a mouse model of acid aspiration-induced lung injury, which may serve as a reliable model for longitudinally studying pulmonary immune-inflammatory mechanism in humans.
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Aim To clone and express the 1.2kb cDNA fragment (1/753-2 934bp) of human integrin α 4 subunit. Methods The 1.2 kb cDNA fragment of human integrin α 4 subunit was amplified from HL-60 total RNA by RT-PCR, then it was subcloned into expression vector pGEX-3X and induced with IPTG. Results The 1.2 kb cDNA fragment of human integrin α 4 subunit was cloned. The sequencing indicated that there was only one missense mutation (Arg→ Gln) among the fragment, and this mutation won't affect antigenicity after analysed by GOLDKEY. Then the 1.2 kb cDNA was subcloned into expression vector pGEX-3X. The α 4 fragment was highexpressed in E.coli after induced with IPTG. Conclusion The 1.2kb cDNA fragment of α 4 subunit was obtained, and it was highexpressed in E.coli, it might be important for study on the function of α 4 integrins.