Objective To investigate the influence of salmeterol with fluticasone on airway inflammation of patients with acute exacerbation chronic obstructive pulmonary disease (COPD).Methods 40 COPD patients in the stage of acute exacerbation were randomly divided into salmeterol with fluticasone group( A group) and controll group (B group).Bronchial alveolar lavage( BAL) was performed as usual.The concentrations of IL-8 and TNF-α in bronchial alveolar lavage fluid(BALF) were measured by ELISA.The results were compared with that of 18 healthy volunteers.Results The levels of IL-8 and TNF-a in BALF of patients in A group(10.60 ± 1.42) μg/L, (14.80 ± 2.05) μg/Land B group( 10.77 ± 1.98) μg/L, (14.70 ± 2.03) μg/L were significantly higher than that of C group (3.40 ±0.65)μg/L, (4.67 ± 1.01) μg/L( all P <0.01) ;Before treatment,the levels of IL-8 and INF-α in BALF of A group( 10.60 ± 1.42)μg/L,(14.80 ±2.05) μg/L and B group( 10.77 ± 1.98) μg/L,(14.70 ±2.03) μg/L had no significant differences (all P > 0.05) ,and the concentrations of IL-8 and TNF-a in BALF in group A (4.39 ± 0.92)μg/L,(5.84 ±1.26) μg/L were significantly lower than that in group B(9.69 ± 1.43) μg/L, (12.88 ± 2.51) μg/L after two weeks treatment ( all P < 0.01).Conclusion Salmeterol with fluticasone could inhibit airway inflammation of COPD patients in the stage of acute exacerbation.

Increased intestinal barrier permeability, leaky gut, has been reported in patients with autism. However, its contribution to the development of autism has not been determined. We selected dextran sulfate sodium (DSS) to disrupt and metformin to repair the intestinal barrier in BTBR T⁺tf/J autistic mice to test this hypothesis. DSS treatment resulted in a decreased affinity for social proximity; however, autistic behaviors in mice were improved after the administration of metformin. We found an increased affinity for social proximity/social memory and decreased repetitive and anxiety-related behaviors. The concentration of lipopolysaccharides in blood decreased after the administration of metformin. The expression levels of the key molecules in the toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-nuclear factor kappa B (NF-κB) pathway and their downstream inflammatory cytokines in the cerebral cortex were both repressed. Thus, "leaky gut" could be a trigger for the development of autism via activation of the lipopolysaccharide-mediated TLR4-MyD88-NF-κB pathway.
Mice ; Animals ; NF-kappa B ; Myeloid Differentiation Factor 88/metabolism* ; Lipopolysaccharides/pharmacology* ; Toll-Like Receptor 4/metabolism* ; Autistic Disorder/metabolism* ; Signal Transduction/physiology*