RESUMO
Immunosuppressed patients are more likely to suffer from pneumonia, especially Streptococcus and Enterobacter pneumonia. Studies have demonstrated the existence of a complex and dynamic microbiota on the surface of human respiratory epithelial cells, both in healthy and diseased states. However, it is not clear whether the pneumonia in immunosuppressed patients is caused by inhaled oropharyngeal pathogens or abnormal proliferation of pulmonary proteobacteria. In this study, immunosuppressed model was made by intraperitoneal injection of cyclophosphamide and oropharyngeal saliva aspiration was simulated by oral and pharyngeal tracheal instillation of sterilized phosphate buffered saline (PBS). Furthermore, the effects of immunosuppression on the lung microbial community and its metabolism were investigated using 16S rRNA gene sequencing and liquid chromatography-mass spectrometry (LC-MS) metabolomics analysis. The 16S rRNA gene sequencing results showed that immunosuppression alone did not change the composition of pulmonary bacteria. Moreover, although the bacteria brought by sterilized PBS from oropharynx to lower respiratory tract changed the composition of the microflora in healthy and immunosuppressed rats, the change in the latter was more obvious. Metabolomic analysis revealed that the levels of pulmonary metabolites were disturbed in the immunosuppressed rats. The altered lung microbiota, including Streptococcaceae and Enterobacteriaceae, showed significant positive correlations with pulmonary metabolites. Our study suggested that the source of the pathogens of pneumonia in immunosuppressed rats was via inhalation and explored the relationship between lung microbiome and metabolites in immunosuppressed rats. Our results provide the basis for the development of prevention and treatment strategies for pneumonia.
RESUMO
An unhealthy diet has been linked to increased incidence of chronic diseases. To investigate the relationship between diet and intestinal inflammation, mice in two experimental groups were fed on a high-fat diet or high-fructose diet, respectively. The result showed that the defecation volume of the experimental groups was significantly reduced compared with that of the control group, and the levels of pro-inflammatory cytokines (interleukin (IL)-1ß and IL-6) and IgG in serum were increased significantly. In addition, inflammatory cell infiltration was observed in intestinal tissue, indicating that a high-fructose or high-fat diet can lead to constipation and inflammation. Further analysis showed that the microbial composition of the experimental groups changed significantly, including a decrease of the Bacteroidetes/Firmicutes ratio and increased levels of Bacteroides, Akkermansia, Lactobacillus, and Ruminococcus, which might be associated with inflammation. The results of pro-inflammatory metabolites analysis showed that the levels of arachidonic acid, stearic acid, and indoxylsulfuric acid were significantly increased in the experimental groups, which were related significantly to Bacteroides, Enterococcus, and Akkermansia. Meanwhile, the content of 5-hydroxytryptamine (5-HT) was significantly decreased, which might cause constipation by reducing intestinal peristalsis. Moreover, transplantation of fecal bacteria from inflammatory mice caused constipation and inflammation in normal mice, which could be relieved by feeding a normal diet. The results of the present study indicated that changes in intestinal microbiota and microbial metabolites may underlie chronic intestinal inflammation and constipation caused by high-fructose and high-fat diets.