S100A8 (S100 Calcium Binding Protein A8)

We identified seven genes that are persistently upregulated during the progression from HC to UC and CAC. These genes influence neutrophils and inflammatory/tumorigenic pathways. The upregulation of PD-L1 in neutrophils suggests that neutrophil-mediated immune suppression may contribute to CAC progression, supporting their potential as molecular markers and therapeutic targets for early intervention in UC-related cancer.

Furthermore, E171-induced secretion of S100A8 and S100A9 in macrophages was suppressed by specific inhibitors, including N-acetylcysteine (NAC, ROS inhibitor), MCC950 (NLRP3 inhibitor), Z-YVAD-FMK (caspase 1 inhibitor), disulfiram (GSDMD inhibitor), and transfection of NLRP3 small interfering ribonucleic acid (siRNA). These results indicate that dietary E171 promotes CAC development by activating macrophages, with S100A8 and S100A9 serving as key mediators, and the NLRP3/caspase 1/GSDMD pathway acting as a critical mechanism.

BALB/C mice were randomized into an NA group, a dexamethasone intervention group (DI, 1 mg/kg), and a Fasudil intervention group (FI, 40 mg/kg). Fasudil ameliorates NA via regulating M1 macrophage polarization, inhibiting the NF-κB/TLR-2/RPS3 pathway, and reducing pro-inflammatory cytokines, with S100A8/A9 and CXCL2 as potential biomarkers. These findings support Fasudil as a promising NA therapy, warranting further clinical translational research.

In patients with IBC, high serum levels of S100A8/A9 are an independent prognostic factor for brain metastasis and poor clinical outcomes. These findings support the potential of S100A8/A9 as predictive biomarker for identifying increased risk of brain metastasis and unfavorable prognosis in patients with IBC.

Blocking S100a9 with tasquinimod rescues the defects of Sucnr1 knock-out mice, and combined with a potent Sucnr1 agonist shows therapeutic value in AML mice...Together, Sucnr1 signaling restricts hematopoiesis at least partially through HSPC and via control of S100a8/S100a9. Its dysregulation emerges as contributor to malignancy that opens therapeutic avenues for AML patients.

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This trimer stabilizes STAT3-enhancer-promoter loops (EPLs), thereby reinforcing the Tns1 transcription and facilitating CRCLM. Our findings elucidate the mechanism by which E. coli-induced NETs promote CRCLM through epigenetic modifications, offering an insight into the role of EPLs in immune regulation and tumor progression.

P=N/A, N=500, Active, not recruiting, University Hospital, Bordeaux | Recruiting --> Active, not recruiting

P=N/A, N=80, Not yet recruiting, Children's Hospital of Chongqing Medical University; Children's Hospital of Chongqing Medical University

IL-18 emerged as a critical inflammatory mediator, with elevated plasma levels correlating with the transformation to high-grade fibrosis (reticulin grades 2-3). Functional assays confirmed that the IL-18 stimulation of mesenchymal stromal cells induced fibrotic transformation, emphasizing its role as a biomarker and target.

Univariate ROC analyses identified S100A6+ plasmacytoid DCs, S100A8+ plasmacytoid DCs, and CD14+CD86+S100A8+ monocytes as candidate PDAC-associated immune features. However, further validation incorporating benign pancreatic conditions and multivariable modeling is required before conclusions can be drawn regarding diagnostic specificity and clinical applicability.

These findings offer preliminary clues for future risankizumab-based combination strategies in psoriasis.