Long-term chronic stress is an important factor in the poor prognosis of cancer patients. Chronic stress reduces the tissue infiltration of immune cells in the tumor microenvironment (TME) by continuously activating the adrenergic signaling, inhibits antitumor immune response and tumor cell apoptosis while also inducing epithelial-mesenchymal transition (EMT) and tumor angiogenesis, promoting tumor invasion and metastasis. This review first summarizes how adrenergic signaling activates intracellular signaling by binding different adrenergic receptor (AR) heterodimers. Then, we focused on reviewing adrenergic signaling to regulate multiple functions of immune cells, including cell differentiation, migration, and cytokine secretion. In addition, the article discusses the mechanisms by which adrenergic signaling exerts pro-tumorigenic effects by acting directly on the tumor itself. It also highlights the use of adrenergic receptor modulators in cancer therapy, with particular emphasis on their potential role in immunotherapy. Finally, the article reviews the beneficial effects of stress intervention measures on cancer treatment. We think that enhancing the body's antitumor response by adjusting adrenergic signaling can enhance the efficacy of cancer treatment.

Chronic obstructive pulmonary disease is a kind of chronic lung disease characterized by persistent air flow obstruction, which was the third leading cause of death in China. The incidence of COPD is steadily and increasing and has been a globally sever disease. Accordingly, it is urgently needed to explore how to diagnose and treat COPD timely. This study aims to find key genes to diagnose COPD as soon as possible to avoid COPD processing and analyze immune cell infiltration between COPD early stage and late stage. Two GEO datasets were merged as the merge data for analyses. 157 DEGs were used for GSEA analysis to find the pathway between COPD early stage and late stage. Above all, gene EXPH5 stood out from the screen as the most likely candidate diagnosis biomarker of COPD indicating the late-stage by least LASSO and SVM-RFE. ROC curves of EXPH5 were applied to represent the discriminatory ability through the area under the curve which is the gold standard to evaluate the accuracy of diagnosis and survival rate. The CIBERSORT algorithm was used to assess the distribution of tissue-infiltrating immune cells between two COPD stages. The diagnosis biomarker, gene EXPH5 had a positive correlation with NK cells resting; mast cell resting, eosinophils, and negative correlation with T cell gamma delta, macrophages M1, which underscore the role of gene and immune cell infiltration. To make results more reliable, we further analyzed the gene EXPH5 expression in single-cell transcriptome data and showed again that EXPH5 genes significantly downregulated in the late stage of COPD especially in the main lung cell types AT1 and AT2. In a word, our study identified genes EXPH5 as a marker gene, which adds to the knowledge for clinical diagnosis and pharmaceutical design of COPD.

Objective: Latent tuberculosis infection (LTBI) may be a risk of developing tuberculosis (TB) and thus a health hazard. The aim of this meta-analysis is to explore the association between vitamin D and LTBI. Methods: Databases including PubMed, Embase, Scopus, and ProQuest were electronically searched to identify observational or interventional studies that reported the association between vitamin D and LTBI. The retrieval time is limited from inception to 30 September 2021. Two reviewers independently screened literature, extracted data, and assessed risk bias of included studies. Meta-analysis was performed by using STATA 12.0 software. Results: A total of 5 studies involving 2 case–control studies and 3 cohort studies were included. The meta-analysis result showed that the risk of LTBI among individuals was not associated with high vitamin D level (OR 0.51, 95% CI 0.05–5.65, P = 0.58). The result from cohort studies also suggested that relatively high vitamin D level was not a protective factor for LTBI (RR = 0.56, 95%CI 0.19–1.67, P = 0.300). Conclusions: Our meta-analysis suggested that serum vitamin D levels were not associated with incidence of LTBI, and relatively high serum vitamin D level was not a protective factor for LTBI. Further RCTs are needed to verify whether sufficient vitamin D levels and vitamin D supplementation reduces the risk of LTBI.

S: Idiopathic pulmonary fibrosis (IPF) is a chronic disease of unknown etiology that lacks a specific treatment. In IPF, macrophages play a key regulatory role as a major component of the lung immune system, especially during inflammation and fibrosis. However, our understanding of the cellular heterogeneity and molecular characterization of macrophages in IPF, as well as their relevance in the clinical setting, is relatively limited. In this study, we analyzed in-depth single-cell transcriptome sequencing (scRNA-seq) data from lung tissues of IPF patients, identified macrophage subpopulations in IPF, and probed their molecular characteristics and biological functions. hdWGCNA identified co-expressed gene modules of a subpopulation of IPF-associated macrophages (IPF-MΦ), and probed the IPF-MΦ by a machine-learning approach. hdWGCNA identified a subpopulation of IPF-associated macrophage subpopulations and probed the IPF-MΦ signature gene (IRMG) for its prognostic value, and a prediction model was developed on this basis. In addition, IPF-MΦ was obtained after recluster analysis of macrophages in IPF lung tissues. Coexpressed gene modules of IPF-MΦ were identified by hdWGCNA. Then, a machine learning approach was utilized to reveal the characteristic genes of IPF-MΦ, and a prediction model was built on this basis. In addition, we discovered a type of macrophage unique to IPF lung tissue named ATP5-MΦ. Its characteristic gene encodes a subunit of the mitochondrial ATP synthase complex, which is closely related to oxidative phosphorylation and proton transmembrane transport, suggesting that ATP5-MΦ may have higher ATP synthesis capacity in IPF lung tissue. This study provides new insights into the pathogenesis of IPF and provides a basis for evaluating disease prognosis and predictive medicine in IPF patients. Graphical Abstract