ArticleFrontiers in cellular and infection microbiology2026
Temporal upregulation of TREM2 parallel to M2 macrophage marker expression in tuberculosis: implications for macrophage polarization regulation.
Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- A review of bloodstream infections-pathogens, pathogenesis, diagnostic strategies, treatment methods-challenges and future aspects.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
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10 authors.
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Abstract
Background: This study aims to explore the association between Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) expression and tuberculosis pathogenesis, with particular focus on its potential correlation with established macrophage polarization markers. Methods: The inflammatory pathology of lung tissues in mock-infected mice was evaluated using hematoxylin and eosin (H&E) staining. Additionally, the expression and localization of M1/M2 macrophage-specific markers and TREM2 were assessed via immunohistochemical (IHC) staining. The expression levels and localization of M1/M2 macrophage-associated cytokines, including IL-10 and IL-6, were measured in peripheral blood using enzyme-linked immunosorbent assay (ELISA) and quantitative real-time PCR (qRT-PCR). Results: I In the experimental group of mice, lung lesions exhibited widened alveolar septa, interstitial edema, and extensive infiltration of inflammatory cells and erythrocytes. TREM2 and inflammatory markers (iNOS and IL-10) showed significant positive expression in the infected lung tissues. Compared to the control group, the Mycobacterium-infected mouse model displayed significantly higher mRNA expression levels of TREM2, along with increased IL-10 and IL-6 production. Following co-culture with Conclusion: TREM2 expression was significantly upregulated in lung tissues of tuberculosis-infected murine models, correlating strongly with increased expression of macrophage-derived cytokines. Notably,
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