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ObjectivesThe aim of this study was to observe the depression-like behavior changes of rats exposed to lead with or without probiotic intervention, and to investigate changes in the gut microbiota and fecal short-chain fatty acids (SCFAs) levels after lead exposure, and the possible functions of probiotics in this process.Material and MethodsAdult male Sprague Dawley rats were exposed to a 300 mg/l lead acetate solution for 24 weeks, with or without probiotic (freeze-dried powder containing Lactobacillus and Bifidobacterium: 6 billion live bacteria/2 g) intervention in weeks 17–24. The sucrose preference test (SPT), the forced swim test (FST), and the tail suspension test (TST) were preformed to study the depression-like behaviors of these rats. The alteration of rat gut microbiota induced by lead exposure was analyzed by 16S rRNA sequencing, and the levels of fecal SCFAs were detected using gas chromatography.ResultsNeurobehavioral tests showed that lead exposure induced depression-like behavior in rats, including reduced sucrose preference in the SPT, and increased immobility times in the FST and the TST. Sequencing and gas chromatography showed that lead exposure changed the structure and the phylogenetic diversity of the gut microbiota, as well as significantly altered the levels of SCFAs. Moreover, the depression-like behaviors, and the changes in both gut microbiota and SCFAs, could be mitigated by probiotic intervention.ConclusionsLead exposure not only changes the structure and diversity of the gut microbiome but also affects metabolic function. Probiotic intervention may be a novel initiative for the prevention and treatment of neurological damage following lead exposure. Health. 2022;35(1):95–106
EN
Objectives The aim of the paper is to explore the role of lung microbiome disorder in lung tissue injury induced by exposure to particulate matter with a maximum diameter of 2.5 μm (PM2.5) and the alleviation effect of auricularia auricular-judae polysaccharide (AAP). Material and Methods Sprague Dawley rats were given PM2.5 suspension at a dose of 20 mg/l twice a week for 8 weeks. Then, 100 mg/kg or 200 mg/kg of AAP was administered to the rats after PM2.5 exposure. The bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected at the end of the experiment. The BALF was meant to detect changes in lung microbiome by 16S sequences and cluster analysis, with the application of the principal component analysis and the partial least squares discriminant analysis. The levels of interferon-γ (IFN-γ), and interleukin (IL)-4, IL-8, and IL-10 in lung tissue were detected by the enzyme-linked immunosorbent assay method. The pathological changes in lung tissue were observed by hematoxylin and eosin staining. Results After PM2.5 exposure, the alveolar septum was widened, and the structures of alveolar walls were destroyed. There was inflammatory cells infiltration in the alveolar space and the interstitial space. Alpha diversity in BALF showed that the Chao1, ACE, Simpson, and Shannon values were increased, and the lung microbiome analysis revealed that the relative abundance of Firmicutes and Clostridium increased, while the relative abundance of Bacteroidetes and Akkermansia decreased. The contents of IFN-γ and IL-8 in lung tissue increased while the content of IL-10 decreased. After the administration of AAP, the alveolar structure damage was alleviated, and the interstitial hemorrhage, edema, and inflammatory cells infiltration were reduced. The Chao1 and ACE values decreased, and the taxonomic abundance values of Akkermansia were much higher. Simultaneously, the contents of IFN-γ, IL-4, and IL-8 decreased, and the content of IL-10 increased. Conclusions It was found that PM2.5 resulted in lung microbiome disorder, which might lead to the inflammation of lung tissue. It was also revealed that AAP could alleviate the inflammatory damage of lung tissue induced by PM2.5.
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