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Related Experiment Video

Updated: Jan 10, 2026

Microfluidics in Assessing Platelet Function
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Toll-like Receptor 7 Deficiency Attenuates Platelet Dysfunction in Sepsis.

Rashida Mohamed-Hinds1, Arijit Dutta1, Chanhee Park1

  • 1Translational Research Program, Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Biomolecules
|November 27, 2025
PubMed
Summary
This summary is machine-generated.

Toll-like Receptor-7 (TLR7) signaling exacerbates sepsis-induced platelet dysfunction and extracellular vesicle (EV) activity. Deficiency in TLR7 preserves platelet function and reduces pathogenic EV effects, indicating TLR7 as a therapeutic target.

Keywords:
Toll-like receptor 7extracellular vesiclesinflammationplateletssepsissepsis-induced platelet dysfunction

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Area of Science:

  • Immunology
  • Hematology
  • Pathophysiology

Background:

  • Sepsis involves abnormal host response to infection, often leading to thrombocytopenia and platelet dysfunction, which worsen patient outcomes.
  • Toll-like Receptor-7 (TLR7), an innate immune sensor, is implicated in sepsis-related thrombocytopenia.
  • The role of TLR7 in sepsis-induced platelet dysfunction and the impact on extracellular vesicle (EV) bioactivity remain unclear.

Purpose of the Study:

  • To investigate the contribution of TLR7 signaling to platelet dysfunction in sepsis.
  • To determine if TLR7 signaling affects the bioactivity of sepsis-associated extracellular vesicles (EVs).

Main Methods:

  • Sepsis was induced in wild-type and TLR7-deficient mice via cecal ligation and puncture.
  • Platelet function was assessed through aggregation, adhesion, and calcium flux assays.
  • Extracellular vesicles (EVs) were isolated from plasma and their role in platelet-leukocyte aggregate (PLA) formation was evaluated in vitro.

Main Results:

  • Septic platelets exhibited hyperactivation and increased adhesion but impaired aggregation and calcium signaling, indicative of functional exhaustion.
  • TLR7-deficient mice showed preserved platelet aggregation, enhanced adhesion, and maintained calcium release compared to wild-type controls.
  • Sepsis increased plasma EV abundance and size, promoting clot and PLA formation; this EV-mediated platelet activation was reduced when using EVs from TLR7-deficient mice.

Conclusions:

  • Sepsis induces persistent platelet activation and dysfunction, which is partially mitigated by TLR7 deficiency.
  • TLR7 signaling critically modulates the pathogenic activity of EVs in sepsis, impacting platelet function.
  • Targeting TLR7 may offer a therapeutic strategy to preserve platelet function and mitigate adverse outcomes in sepsis.