The role of S100A9 in the progression of tuberculosis

Abstract Objective: Elevated plasma levels of S100A9 have been observed in patients with severe tuberculosis, with further increases in patients with poor prognosis, suggesting that S100A9 is a potential biomarker for disease progression and prognosis. However, the molecular mechanism underlying its potential remains unclear, highlighting the importance of exploring its function. Methods: To further investigate the role of S100A9 in severe tuberculosis, we constructed S100A9 gene knockout or overexpression models and analyzed the transcriptome changes in THP-1 cells following S100A9 overexpression or shRNA silencing using next-generation sequencing. Through the analysis of transcriptome sequencing results, we identified eight genes that may be involved in the regulation of S100A9 expression. We also detected the expression of the S100A9 gene and related differentially expressed genes after Mycobacterium tuberculosisinfection, as well as their enrichment and related pathways. It was inferred that S100A9 may be involved in the mechanism by which tuberculosis progresses to severe tuberculosis. Results: FOSB and IL17c are potentially related to the IL-17 signaling pathway, while calcium/calmodulin-dependent protein kinase II beta (CAMK2B) may be related to the ErbB signaling pathway. These findings indicate that these genes may promote the progression of tuberculosis through different mechanisms. Conclusion: Our study explored the potential role and mechanism of S100A9 in the development of tuberculosis, providing a new perspective for the development of treatment strategies for this disease.