ObjectiveTo investigate the effect of Lactobacillus plantarum (LP) on the intestinal barrier function under inflammation. MethodsInterleukin-10 knockout (IL-10－/－) mice were used as the model of inflammatory bowel disease. IL-10－/－ and wild type (WT) mice received the LP or Ringer solutions for 4 weeks. Colitis was assessed by histological score and clinical manifestation was observed. The gut paracellular permeability was measured by Ussing chamber. The concentrations of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) were detected by the ELISA method. The expressions and distributions of tight junction proteins were determined by Western blot and immunofluorescence, respectively. ResultsCompared with the WT group, the diarrhea, rectal prolapse, and weight loss were obvious (Plt;0.01), the concentrations of TNF-α and IFN-γ significantly increased (Plt;0.01), the infiltration of numerous inflammatory cells, even transmural ulcers, and crypt abscess were observed, the ultrastructure of tight junction was damaged, the mannitol permeability significantly increased (Plt;0.001) and transepithelial resistance (TER) significantly decreased (Plt;0.001), and the expressions of tight junction proteins (ZO-1, occludin, and claudin-1) significantly decreased (Plt;0.01) in the IL-10－/－ group. Compared with the IL-10－/－ group, the clinical and pathological manifestations of colitis significantly improved (Plt;0.01), the ultrastructural damage of tight junction was prevented, the mannitol permeability significantly decreased (Plt;0.001) and the TER significantly increased (Plt;0.001), the concentrations of TNF-α and IFN-γ significantly decreased (Plt;0.01), and the expressions of tight junction proteins (ZO-1, occludin, and claudin-1) significantly increased (Plt;0.01) in the IL-10－/－+LP group. ConclusionTreatment with LP ameliorates colonic epithelial barrier dysfunction by promoting the expressions of tight junctional proteins in IL-10－/－ mice.
ObjectiveTo investigate the effects of acute and chronic ozone exposure on inflammation,structure and function in murine lung. Methods32 C57/BL6 mice were randomly divided into a single (acute) ozone exposed group,a single air exposed group,a multiple (chronic) ozone exposed group (every three days over 6 weeks),and a multiple air exposed group with 8 mice in each group.The mice were exposed to 2.5 ppm of ozone or air for 3 hours per time and sacrificed 24 hours after the last time of ozone exposure.Lung volume,low attenuation area (LAA) percentage,lung function,cell counts and malondialdehyde (MDA) in bronchoalveolar lavage fluid (BALF),8-hydroxy-2'-deoxyguanosine (8-OHdG) in serum,inflammation scores and mean linear intercept (Lm) in lung section were assessed. ResultsCompared with the single air exposed group,single (acute) ozone exposure led to increases in inflammatory cells in BALF,inflammation scores in the lung tissue,MDA in BALF and 8-OHdG in serum,but had no effect on lung volume,LAA percentage,airflow or Lm.Compared with the single (acute) ozone exposed group,the single air exposed group and the multiple air exposed group,multiple (chronic) ozone exposure increased inflammatory cells in BALF,lung volume,LAA percentage,total lung capacity and lung compliance,mediated airflow obstruction,and also increased lung inflammation socres and Lm. ConclusionAcute ozone exposure induced airway/lung inflammation and oxidative stress,while chronic ozone exposure induced airway/lung inflammation,emphysema and airflow obstruction.