Potential Role of Neutrophil-Platelet Interaction in Increased Susceptibility to Infection of Patients with Down Syndrome

Abstract

Objective Recurrent infection in Down syndrome (DS) has been previously documented; the potential role of platelets and neutrophil-platelet interaction has not been addressed in previous studies. Patients and Methods Using flow cytometry, we evaluated CD40 and CD18 expression as activation markers for neutrophils and CD62p as an activation marker for platelets, before and after lipopolysaccharide (LPS) stimulation, in 34 patients with DS and 39 control patients. Results Markers were evaluated as percentage of positivity, mean fluorescent intensity (MFI), and activation index (MFI after stimulation/MFI before stimulation). Patients showed a significantly lower CD40 MFI (P = .019) after LPS stimulation, a lower CD62p percentage before and after LPS stimulation (P = .013 and P = .029), and a higher CD62p MFI (P = .011) after LPS stimulation. Patients showed a lower activation index for CD40 and CD18 (P ≤ .001) but not for CD62p (P = .338). Dysfunctional efficiency in neutrophils and in the neutrophil-platelet interaction could not be correlated to infection. Conclusion A consensus on a scoring system for infection is needed for an objective evaluation of correlation to infection.

Elevated Preoperative NMPR Predicts an Unfavorable Chance of Survival in Resectable Esophageal Squamous Cell Carcinoma

“…The direct and indirect interplay between platelet and neutrophil was able to regulate several aspects of tumor-associated pathology and influence the tumor immune microenvironment in cancer at various stages [33]. Further mechanistic investigation demonstrated that platelets might augment rolling and firm neutrophil adhesion via the crosstalk between platelets and neutrophils initiated by the platelet surface marker P-selectin (CD62P) and neutrophil surface marker P-selectin-binding glycoprotein 1 (PSGL-1) [34,35]. Subsequently, plateletneutrophil interaction fostered mutual activation and neutrophil extracellular traps and triggered the release of platelet granule contents and the generation of lipid mediators, which affected the functions of various effector immune cells including T-helper, CD8+ T and natural killer cells in the tumor environment via various cytokines, chemokines and prostaglandins signaling such as Toll-like receptors, interleukin-1 (IL-1), IL-17, CCL2, IL-8, PD-L1, IFN-γ, and TNF-α, etc., facilitating immune evasion of cancer cells and tumor development and dissemination [33].…”