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Abstract Background Differentially expressed genes/proteins (DEGs/DEPs) play critical roles in pulmonary tuberculosis (PTB) diagnosis and treatment. However, there is a scarcity of reports on DEGs/DEPs in lung tissues and blood samples in PTB patients. Objective We aim to identify the DEGs/DEPs in lung tissues and blood samples of PTB patients and investigate their roles in PTB. Materials and Methods The lung granulomas and normal tissues were collected from PTB patients for proteomic and transcriptomic analyses. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses annotated the functions of DEGs/DEPs. The GSE107994 data set was downloaded to identify the DEGs/DEPs in peripheral blood. The common DEGs and DEPs were identified. A nomogram was established. Pearson correlation analysis was conducted. Results Eighty‐three DEGs/DEPs were identified. These DEGs/DEPs were mainly enriched in the movement of cell or subcellular components, regulation of cellular component biogenesis, and actin filament‐based process as well as in the pathways of inositol phosphate metabolism, adherens junction, phosphatidylinositol signaling system, leukocyte transendothelial migration, regulation of actin cytoskeleton, and tight junction. There were eight common DEGs/DEPs (TYMP, LAP3, ADGRL2, SIL1, LMO7, SULF 1, ANXA3, and PACSIN3) between the lung tissues and blood samples. They were effective in predicting tuberculosis. Moreover, the activated dendritic cells, macrophages, monocytes, neutrophils, and regulatory T cells were significantly positively correlated with TYMP (r > .50), LAP3 (r > .50), SIL1 (r > .50), ANXA3 (r > .5), and PACSIN3 (r .05). Limitations The sample size was small. Conclusions Eight common DEGs/DEPs of lung tissues and blood samples were identified. They were correlated with immune cells and demonstrated predictive value for PTB. Our data may facilitate the diagnosis and treatment of PTB.

Effects of octenylsuccinate (OS) starch on body composition and intestinal environment in high-fat diet-fed mice were investigated. C57BL/6J mice were treated with a regular-fat (RF) diet, a high-fat (HF) diet, or a high-fat diet supplemented with OS starch (HFOSS). Fecal short-chain fatty acids (SCFAs) were quantified using gas chromatography, and the fecal microbiota profile was analyzed by 16S rDNA sequencing. One-way ANOVA and metastats analysis were performed for statistical analysis. After 22 weeks of feeding, mice in the HFOSS group had significantly lower body weight, body fat, liver weight, and cumulative food intake than those in the HF group but higher than that of the RF group. Fecal total SCFA, acetic, propionic, and butyric acid concentrations were significantly higher in the HFOSS group than that in the HF and RF groups. OS starch intervention increased the relative abundance of Parabacteroides, Alistipes, and Ruminiclostridium_5 and decreased that of Tyzzerella, Oscillibacter, Desulfovibrio, and Anaerotruncus compared with the RF and HF groups. The relative abundance of Lachnospiraceae_UCG-006 in the HFOSS group was lower than that in the HF group but higher than that in the RF group. In conclusion, OS starch prevents fat accumulation in high-fat diet-fed mice and might provide potential health benefits due to its fermentability in the gut and its ability to regulate gut microbial community structure.