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Transcriptomic Insights into Human Macrophage Responses to Mycobacterium tuberculosis Complex (MTBC) Strains

J Schönfeld(1) C Utpatel(1,3) V Dreyer(1,3) T Dallenga(3,4) S Niemann(1,2,3)

1:Molecular and Experimental Mycobacteriology, Research Center Borstel Leibniz Lung Center; 2:National Reference Center, Research Center Borstel Leibniz Lung Center, Borstel, Germany; 3:German Centre for Infection Research, Partner Site Hamburg-Lübeck-Borstel-Riems, Borstel, Germany; 4:Cellular Microbiology, Research Center Borstel Leibniz Lung Center, Borstel, Germany

Tuberculosis, caused by various strains of the Mycobacterium tuberculosis complex (MTBC), remains a leading cause of mortality globally, necessitating innovative approaches to better understand the host-pathogen interaction. Macrophages play a pivotal role in MTBC infection, serving as both hosts and effectors in the immune response. Results of previous studies indicate that MTBC infection can lead to detrimental epigenetic reprogramming. Understanding the transcriptomic response of human macrophages to different MTBC strains is one step in identifying epigenetic alterations caused by MTBC.

In our study, we aim to investigate the changes in the epigenetic makeup of human macrophages during early-stage MTBC infection. As a first step, we analyze gene expression data of human macrophages infected with diverse MTBC strains to elucidate the differential host-pathogen interactions at the molecular level. This part of the investigation focuses on the variations in gene expression profiles, which could provide insights into strain-specific immune evasion mechanisms. Data analysis involves differential gene expression analysis, pathway enrichment, and network analysis to identify key regulatory mechanisms activated by different MTBC strains.

We anticipate identifying distinct transcriptional signatures associated with different MTBC lineages. These signatures might highlight differences in immune response modulation, providing a deeper understanding of MTBC pathogenesis and host defense strategies.

This study promises to advance our understanding of MTBC-host interactions and tuberculosis pathophysiology.

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