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Gene expression analysis across the inflammatory models: A step towards biomarker discovery

Dr.H S Santosh Kumar Associate Professor, Department of Biotechnology, Kuvempu University, Karnataka, India Deepthi S Ph.D. Student, Department of Biotechnology, Kuvempu University, Karnataka, India

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Inflammation serves as the body's primary defense mechanism against infections and tissue injuries; however, when it becomes chronic, it can have detrimental effects. Balancing the beneficial aspects of inflammation with the potential for long-term tissue damage is crucial. Achieving this balance necessitates early diagnosis and clinical differentiation of various inflammatory conditions, which is challenging due to the complex pathophysiological and genetic characteristics of inflammatory cascades. So, it is the need of the hour to identify the condition-specific biomarkers for inflammation. This study aims to conduct a preliminary analysis of gene expression profiles for three different inflammatory conditions: sepsis, trauma, and anaphylaxis. By retrieving and sorting significant differentially expressed genes (DEGs) (p-value < 0.05) for each condition, the common and exclusive genes among the 3 conditions were identified and listed along with their logFC value. Furthermore, the condition-specific DEGs were employed to construct a protein-protein interaction network, and hub genes were identified based on Cytoscape network parameters. Subsequently, gene enrichment analysis was performed. Among the three conditions studied, a total of 1530 common genes with significantly varied expressions were identified. The hub genes, including AKT1, SRC, TP53, TNF, MAPK3, EGFR, EP300, UBC, CTNNB1, RPS27A, HDAC1, CREBBP, and others, were found to be common among the conditions but exhibited distinct expression patterns. Enriched pathways such as the TNF signaling pathway and the C-type lectin receptor signaling pathway were up-regulated in sepsis (LPS-induced), while being down-regulated in the trauma condition. Conversely, the inflammatory mediator regulation of TRP channels pathway was up-regulated in trauma and down-regulated in sepsis. Moreover, the MAPK signaling pathway was down-regulated, while autophagy was up-regulated in the anaphylaxis condition. A more comprehensive understanding of these specific inflammatory responses will provide a holistic view and facilitate the identification of biomarkers that may offer therapeutic or diagnostic insights.

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