# Diagnostic value of procalcitonin and hemocyte parameters in neonates with bloodstream infection: Role of activated hemocyte‐related genes

## TL;DR

This study shows that combining blood cell markers and procalcitonin can accurately detect bloodstream infections in newborns, with bioinformatics revealing key genes involved in immune response.

## Contribution

The study introduces a novel predictive model and identifies a gene network (SPI1-TYROBP-FCER1G) linked to neonatal sepsis.

## Key findings

- A predictive model achieved 96.8% accuracy in diagnosing neonatal bloodstream infections.
- Lymphocyte, PDW, PLR, and PCT were identified as independent predictors of BSI.
- SPI1, TYROBP, and FCER1G genes were found to be co-expressed and linked to immune cell activation in sepsis.

## Abstract

This study aimed to evaluate the diagnostic potential of hemocyte parameters and procalcitonin (PCT) in detecting bloodstream infections (BSI) in neonates and explore the contribution of hemocyte activation‐related genes to pediatric sepsis through bioinformatics analysis. A cohort of 419 neonates, categorized as BSI (positive blood culture) and control, underwent comparative analysis of PCT and hemocyte parameters. A predictive model for neonatal BSI was established, demonstrating an impressive area under the receiver ROC curve of 0.968 with remarkable sensitivity (92%) and specificity (87.3%). Hemocyte parameters, including lymphocyte and neutrophil percentages, platelet distribution width (PDW), platelet to lymphocyte ratio (PLR), and PCT, emerged as independent predictors of neonatal BSI. Furthermore, bioinformatics analysis utilizing Gene Expression Omnibus (GEO) datasets yielded significant insights. Differential gene expression (DEGs), gene ontology (GO), pathway enrichment, gene set enrichment analysis (GSEA), and protein–protein interaction (PPI) networks were explored. The differentially expressed genes and hub genes were notably enriched in the activation of neutrophils, lymphocytes, and platelets. Notably, elevated expression levels of SPI1, TYROBP, and FCER1G were observed in pediatric sepsis or septic shock, with positive correlations between SPI1, FCER1G, and TYROBP. In summary, the combination of lymphocyte, PDW, PLR, and PCT effectively diagnosed neonatal BSI. Bioinformatics analysis underscored the pivotal role of activated hemocytes in diagnosing pediatric sepsis, with SPI1, TYROBP, and FCER1G co‐expression influencing the disease's pathophysiology by modulating neutrophil and platelet activity.

Our model, incorporating accessible biomarkers (PCT, LY%, NE%, PDW, and PLR), demonstrated enhanced neonatal BSI diagnosis. Our study unveiled the pivotal role of the SPI‐TYROBP‐FCER1G co‐expression network in pediatric sepsis immune response, impacting neutrophil and platelet activation, potentially indicating novel biomarkers.