A pterygium is a common conjunctival degeneration and inflammatory condition. It grows onto the corneal surface or limbus, causing blurred vision and cosmetic issues. Ultraviolet is a well-known risk factor for the development of a pterygium, although its pathogenesis remains unclear, with only limited understanding of its hereditary basis. In this study, we collected RNA-seq from both pterygial tissues and conjunctival tissues (as controls) from six patients (a total of twelve biological samples) and retrieved publicly available data, including eight pterygium samples and eight controls. We investigated the intrinsic gene regulatory mechanisms closely linked to the inflammatory reactions of pterygiums and compared Asian (Korea) and the European (Germany) pterygiums using multiple analysis approaches from different perspectives. The increased expression of antioxidant genes in response to oxidative stress and DNA damage implies an association between these factors and pterygium development. Also, our comparative analysis revealed both similarities and differences between Asian and European pterygiums. The decrease in gene expressions involved in the three primary inflammatory signaling pathways—JAK/STAT, MAPK, and NF-kappa B signaling—suggests a connection between pathway dysfunction and pterygium development. We also observed relatively higher activity of autophagy and antioxidants in the Asian group, while the European group exhibited more pronounced stress responses against oxidative stress. These differences could potentially be necessitated by energy-associated pathways, specifically oxidative phosphorylation.

The LPS-induced inflammation model is widely used for studying inflammatory processes due to its cost-effectiveness, reproducibility, and faithful representation of key hallmarks. While researchers often validate this model using clinical cytokine markers, a comprehensive understanding of gene regulatory mechanisms requires extending investigation beyond these hallmarks. Our study leveraged multiple whole-blood bulk RNA-seq datasets to rigorously compare the transcriptional profiles of the well-established LPS-induced inflammation model with those of several human diseases characterized by systemic inflammation. Beyond conventional inflammation-associated systems, we explored additional systems indirectly associated with inflammatory responses (i.e., ISR, RAAS, and UPR) using a customized core inflammatory gene list. Our cross-condition-validation approach spanned four distinct conditions: systemic lupus erythematosus (SLE) patients, dengue infection, candidemia infection, and staphylococcus aureus exposure. This analysis approach, utilizing the core gene list aimed to assess the model’s suitability for understanding the gene regulatory mechanisms underlying inflammatory processes triggered by diverse factors. Our analysis resulted in elevated expressions of innate immune-associated genes, coinciding with suppressed expressions of adaptive immune-associated genes. Also, upregulation of genes associated with cellular stresses and mitochondrial innate immune responses underscored oxidative stress as a central driver of the corresponding inflammatory processes in both the LPS-induced and other inflammatory contexts.

Objectives: To identify molecular mechanisms distinguishing the erosive subtype of oral lichen planus (EOLP) from the non‐erosive subtype (NEOLP) through transcriptomic analysis. Methods: We analysed bulk RNA‐seq data from 30 buccal mucosa samples (13 EOLP, 17 NEOLP) using differential expression, Gene Set Enrichment Analysis (GSEA), transcription factor inference, bulk transcriptome deconvolution with xCell 2.0, metabolic flux simulation and novel pathway correlation analysis combining Gene Set Variation Analysis (GSVA) with Differential Gene Correlation Analysis (DGCA). Results: Three molecular signatures distinguished EOLP from NEOLP. First, metabolic–inflammatory coordination was disrupted in EOLP, with reversed correlations between integrated stress response regulators and metabolic pathways. Second, EOLP showed concurrent suppression of cell cycle and senescence programs, suggesting an altered epithelial state. Third, inflammatory profiling revealed myeloid‐skewed activation (elevated SPI1/PU.1), enrichment of bacterial‐response pathways, and loss of epithelial barrier signatures (GRHL2, keratinization). Mitochondrial dysfunction with selective Complex IV upregulation further supported a myeloid‐driven metabolic remodelling in EOLP. Conclusions: EOLP is characterised by disrupted metabolic–stress coordination, epithelial dysregulation, and myeloid‐dominant inflammation. Our findings support a model in which microbial‐associated stimuli may drive myeloid‐centred metabolic reprogramming that sustains chronic inflammatory activity in EOLP. These results highlight potential therapeutic axes including restoration of metabolic–inflammatory balance, modulation of microbial influences, and epithelial barrier repair, although validation in larger cohorts and higher‐resolution studies is required.

Recent studies in murine disease models have identified Siglec-F⁺ neutrophils, which express a marker traditionally associated with eosinophils, as a functionally distinct population characterized by extended lifespans and context-dependent roles. While conventional neutrophils typically return to the bone marrow or undergo apoptosis at the site of inflammation, these cells remain in tissues for extended periods. These cells demonstrate remarkable functional plasticity, promote bacterial clearance and immune activation during infections, foster immunosuppression and tumor progression in cancer, and contribute to tissue remodeling in fibrotic diseases. In this review, we examine the key features governing Siglec-F⁺ neutrophil differentiation and function—including Siglec-F signaling, metabolic programming, and upstream cytokine cues—and explore how targeting these pathways may offer promising avenues for precision immunomodulation.