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Inflammation biomarkers and pathways
Research Guide
What is Inflammation biomarkers and pathways?
Inflammation biomarkers and pathways refer to molecular markers such as TREM-1, endocan, and TREM2, along with associated signaling cascades involving myeloid cells, that mediate inflammatory responses in conditions including sepsis, pneumonia, septic shock, and neurodegenerative diseases.
This field encompasses 10,441 published works examining TREM-1 and endocan as biomarkers in inflammatory diseases, with roles in modulating immune cells like macrophages and neutrophils. TREM2 variants and pathways influence microglial dysfunction in Alzheimer's disease and other neurodegenerative conditions. Studies highlight myeloid-derived suppressor cells (MDSCs) and microglial polarization as key regulators in inflammation and sepsis immunopathology.
Topic Hierarchy
Research Sub-Topics
TREM-1 in Sepsis Pathophysiology
This sub-topic delves into the role of TREM-1 receptor in amplifying inflammatory signals during sepsis, focusing on its expression in myeloid cells. Researchers study signaling pathways and therapeutic blockade for septic shock.
Endocan as Endothelial Inflammation Biomarker
This sub-topic examines endocan (ESM-1) as a biomarker of endothelial activation in inflammatory diseases like pneumonia and sepsis. Studies validate its prognostic utility in clinical settings.
Myeloid-Derived Suppressor Cells in Inflammation
This sub-topic investigates MDSCs' regulatory functions in chronic inflammation and sepsis, including their immunosuppressive mechanisms. Research characterizes heterogeneity and therapeutic reprogramming.
Microglial TREM2 in Neuroinflammation
This sub-topic explores TREM2 variants and pathways in microglial activation during neurodegenerative inflammation. Studies link it to Alzheimer's and related diseases.
M1/M2 Macrophage Polarization in Sepsis
This sub-topic analyzes classical (M1) vs. alternative (M2) macrophage polarization in sepsis-induced immune dysregulation. Researchers probe metabolic shifts and pharmacological interventions.
Why It Matters
Inflammation biomarkers like TREM2 enable risk assessment for Alzheimer's disease, where heterozygous rare variants increase disease risk significantly, as shown in 'TREM2 Variants in Alzheimer's Disease' (2012) with 2949 citations. In sepsis, pathways involving cachectin/TNF contribute to lethal bacteraemia and endotoxin effects, where anti-cachectin/TNF monoclonal antibodies prevented septic shock in mice ('Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia', 1987, 2461 citations) and passive immunization protected against endotoxin lethality ('Passive Immunization Against Cachectin/Tumor Necrosis Factor Protects Mice from Lethal Effect of Endotoxin', 1985, 2361 citations). These findings support diagnostic applications for pneumonia and septic shock, and therapeutic targeting in immune-mediated tumour progression via MDSCs ('Recommendations for myeloid-derived suppressor cell nomenclature and characterization standards', 2016, 2630 citations).
Reading Guide
Where to Start
'Myeloid-derived suppressor cells as regulators of the immune system' (2009) by Gabrilovich and Nagaraj, as it provides a foundational overview of MDSCs in immune regulation with 6516 citations, essential for understanding inflammation biomarkers.
Key Papers Explained
'Myeloid-derived suppressor cells as regulators of the immune system' (2009) by Gabrilovich and Nagaraj lays the basis for MDSC roles, extended by nomenclature standards in 'Recommendations for myeloid-derived suppressor cell nomenclature and characterization standards' (2016) by Bronte et al. TREM2 functions build from 'TREM2 Variants in Alzheimer's Disease' (2012) by Guerreiro et al. to pathway details in 'The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases' (2017) by Krasemann et al. Sepsis insights connect 'The immunopathogenesis of sepsis' (2002) by Cohen with therapeutic validations in 'Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia' (1987) by Tracey et al.
Paper Timeline
Most-cited paper highlighted in red. Papers ordered chronologically.
Advanced Directions
Current research emphasizes microglial polarization and metabolic states ('Microglial M1/M2 polarization and metabolic states', 2015) alongside sepsis targets ('The immunopathology of sepsis and potential therapeutic targets', 2017), with no recent preprints available to indicate ongoing refinements in TREM-1, endocan, and MDSC applications.
Papers at a Glance
| # | Paper | Year | Venue | Citations | Open Access |
|---|---|---|---|---|---|
| 1 | Myeloid-derived suppressor cells as regulators of the immune s... | 2009 | Nature reviews. Immuno... | 6.5K | ✕ |
| 2 | <i>TREM2</i> Variants in Alzheimer's Disease | 2012 | New England Journal of... | 2.9K | ✓ |
| 3 | The TREM2-APOE Pathway Drives the Transcriptional Phenotype of... | 2017 | Immunity | 2.8K | ✓ |
| 4 | The immunopathogenesis of sepsis | 2002 | Nature | 2.7K | ✕ |
| 5 | Recommendations for myeloid-derived suppressor cell nomenclatu... | 2016 | Nature Communications | 2.6K | ✓ |
| 6 | Identification of a unique TGF-β–dependent molecular and funct... | 2013 | Nature Neuroscience | 2.5K | ✓ |
| 7 | Anti-cachectin/TNF monoclonal antibodies prevent septic shock ... | 1987 | Nature | 2.5K | ✕ |
| 8 | Passive Immunization Against Cachectin/Tumor Necrosis Factor P... | 1985 | Science | 2.4K | ✕ |
| 9 | Microglial <scp>M1/M2</scp> polarization and metabolic states | 2015 | British Journal of Pha... | 2.0K | ✓ |
| 10 | The immunopathology of sepsis and potential therapeutic targets | 2017 | Nature reviews. Immuno... | 1.8K | ✕ |
Frequently Asked Questions
What role does TREM2 play in inflammation pathways?
TREM2 variants are associated with increased risk of Alzheimer's disease through effects on microglial function. 'TREM2 Variants in Alzheimer's Disease' (2012) identified heterozygous rare variants linked to significant risk elevation. The TREM2-APOE pathway drives transcriptional phenotypes of dysfunctional microglia in neurodegenerative diseases ('The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases', 2017).
How do myeloid-derived suppressor cells function as inflammation biomarkers?
Myeloid-derived suppressor cells regulate immune responses in cancer and pathological conditions. 'Myeloid-derived suppressor cells as regulators of the immune system' (2009) by Gabrilovich and Nagaraj established their regulatory role with 6516 citations. Nomenclature standards confirm their contributions to tumour progression ('Recommendations for myeloid-derived suppressor cell nomenclature and characterization standards', 2016).
What are key pathways in sepsis immunopathogenesis?
Sepsis involves dysregulated immune responses with potential therapeutic targets in inflammation pathways. 'The immunopathogenesis of sepsis' (2002) by Cohen detailed these mechanisms with 2732 citations. Anti-TNF interventions block lethal effects in bacteraemia and endotoxin models ('Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia', 1987).
How does microglial polarization relate to inflammation?
Microglia exhibit M1/M2 polarization influenced by metabolic states in response to injury. 'Microglial M1/M2 polarization and metabolic states' (2015) by Orihuela et al. described their phenotypic diversity with 1954 citations. TGF-β induces a unique molecular signature in microglia ('Identification of a unique TGF-β–dependent molecular and functional signature in microglia', 2013).
What diagnostic potential do TREM-1 and endocan have?
TREM-1 and endocan serve as diagnostic markers for pneumonia, septic shock, and inflammatory diseases. They impact macrophages, neutrophils, and endothelial cells in immune responses. The field includes 10,441 papers focused on these biomarkers.
Open Research Questions
- ? How do TREM2-APOE interactions precisely alter microglial transcriptional profiles in diverse neurodegenerative contexts?
- ? What specific mechanisms link MDSC accumulation to non-immune-mediated contributions in tumour progression?
- ? Which molecular signatures distinguish TGF-β-dependent microglial states across inflammatory diseases?
- ? How can TNF pathway inhibitors be optimized to prevent septic shock without immunosuppression?
- ? What environmental factors drive M1/M2 microglial polarization in sepsis immunopathology?
Recent Trends
The field maintains 10,441 works with a focus on TREM-1 and endocan in sepsis and inflammatory diseases, as no growth rate data or recent preprints/news are available.
Highly cited papers like 'TREM2 Variants in Alzheimer's Disease' (2012, 2949 citations) and 'The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases' (2017, 2770 citations) continue to anchor investigations into microglial pathways.
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