Background. ST-elevation myocardial infarction (STEMI) is a myocardial infarction (MI) with ST-segment exaltation of electrocardiogram (ECG) caused by vascular occlusion of the epicardium. However, the diagnostic markers of STEMI remain little. Methods. STEMI raw microarray data are acquired from the Gene Expression Omnibus (GEO) database. Based on GSE60993 and GSE61144, differentially expressed genes (DEGs) are verified via R software, and key modules associated with pathological state of STEMI are verified by weighted correlation network analysis (WGCNA). Take the intersection gene of key module and DEGs to perform the pathway enrichment analyses by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Construct the protein-protein interaction (PPI) network by Cytoscape. Then, select and identify the diagnostic biomarkers of STEMI by least absolute shrinkage and selection operator (LASSO) logistic regression and support vector machine-recursive feature elimination (SVM-RFE) algorithms. Finally, assess the infiltration of immune cells of STEMI by CIBERSORT and analyze the correlation between diagnostic markers and infiltrating immune cells. Results. We get 710 DEGs in the STEMI group and 376 genes associated with STEMI in blue module. 92 intersection genes were concentrated in 30 GO terms and 2 KEGG pathways. 28 hub genes involved in the development of STEMI. Moreover, upregulated ALOX5AP (AUC = 1.00) and BST1 (AUC = 1.00) are confirmed as diagnostic markers of STEMI. CD8+T cells, regulatory T (Treg) cells, resting natural killer (NK) cells, M0 macrophages, resting mast cells, and neutrophils are related to the procession of STEMI. Moreover, ALOX5AP and BST1 are positively related to resting NK cells, M0 macrophages, and neutrophils, while ALOX5AP and BST1 are negatively related to CD8+ T cells, Treg cells, and resting mast cells. Conclusion. ALOX5AP and BST1 may be the diagnostic markers of STEMI. Immune cell infiltration plays a key role in the development of STEMI.

Background: Neonatal sepsis is an acute life-threatening condition in neonates, and a proper innate inflammatory is essential for prevention of the systemic inflammation associated with sepsis. As the most potential antigen-presenting innate immune cells, dentritic cells (DCs) dysfunction has been verified detrimental for sepsis. B and T lymphocyte attenuator (BTLA) is an immune-regulatory receptor shown to be associated with DCs dysfunction. However, the role of BTLA expression in myeloid DCs (mDCs) in neonatal sepsis is unknown. Methods: 61 of neonates with sepsis and 32 of neonates having no suspicion of sepsis as control were enrolled into this study. BTLA and HLA-DR expression in mDCs was measured by flow cytometry. To further study the role of BTLA in regulating mDCs function, BTLA+mDCs and BTLA-mDCs from septic neonates were sorted and utilized to evaluate the phagacytosis capacity, bactericidal ability as well as cytokine secretion of mDCs.Results: A higher percentage of BTLA+mDCs were observed in neonatal septic patients and the percentage was positively correlated to the duration of hospitalization of neonates as well as the severity of sepsis. Moreover, a decrease MFI expression of HLA-DR was found in mDCs in neonatal sepsis, which expression was negatively correlated with the percentage of BTLA+mDCs. When compared to BTLA-mDCs, sorted BTLA+mDCs exhibited lower FITC-dextran uptake capacity but more CFU E.coli number after cells challenged by E.coli. In addition, BTLA+mDCs comparatively secreted lower level of TNF-α and IL-12, but higher IL-10. Conclusions: A higher level of BTLA in mDCs in the observed septic neonates was associated to the severity of neonatal sepsis; therefore, BTLA expression in mDCs could be a useful biomarker help to determine the neonatal sepsis development. Additionally, BTLA negatively regulated the phagocytosis capacity and bactericidal ability of mDCs and lowered their antigen-presenting ability as well as altered cells into an anti-inflammatory phenotype. Thus, targeting BTLA in mDCs may be a new therapeutic strategy for neonatal sepsis.