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Platelet activation and platelet-monocyte interaction amplify thromboinflammation in obesity through adhesion
Paula R B Dib1, Mayara K C Fernandes1, Letícia A F Venerando2
1Laboratory of Immunothrombosis, Department of Biochemistry, Institute of Biological Sciences, Federal University of Juiz de Fora, Juiz de Fora, Brazil.
Insights
Obesity promotes platelet activation and platelet-monocyte aggregates, contributing to inflammation and cardiovascular risk. This study reveals a reciprocal activation loop driving thromboinflammation in obese individuals.
Area of Science:
- Cardiovascular Research
- Immunology
- Metabolic Disorders
Background:
- Obesity is linked to chronic inflammation and increased cardiometabolic risk.
- Platelets play critical roles in hemostasis, inflammation, and immunity.
- Mechanisms of platelet-leukocyte interactions in obesity-related inflammation are not fully understood.
Purpose of the Study:
- To investigate the role of platelet activation and platelet-leukocyte interactions in obesity-induced inflammation.
- To elucidate the mechanisms underlying thromboinflammation in obesity.
Main Methods:
- Observational cross-sectional study of 87 obese patients (BMI >30).
- Co-culture models to investigate thromboinflammatory amplification mechanisms.
- Evaluation of platelet and monocyte activation markers, including CD16 and tissue factor (TF).
Main Results:
- Obese individuals exhibit increased platelet activation and platelet-monocyte aggregate formation.
- Platelet-monocyte interaction leads to reciprocal activation, TF expression, and pro-inflammatory mediator secretion.
- This activation loop is partially dependent on CD62P, CD40L, and integrin αIIb/β3 signaling.
- Co-culture conditioned medium activates endothelial cells.
Conclusions:
- A reciprocal platelet-monocyte activation loop contributes to thromboinflammation in obesity.
- This loop is associated with cardiometabolic risk markers in obese patients.
- Understanding these mechanisms offers potential therapeutic targets for obesity-related cardiovascular complications.
Background:
Obesity is a global health concern associated with chronic low-grade inflammation that supports high cardiometabolic risk. Proinflammatory and prothrombotic states contribute to the development of cardiovascular diseases, a leading cause of mortality in obesity. Platelets are chief effectors of hemostasis and pathologic thrombosis that have been highlighted for their key roles in inflammation and immunity. Platelets secrete inflammatory mediators and interact with leukocytes, regulating crucial responses. However, the mechanisms and functional responses of platelet-leukocyte aggregates in obesity and their link to chronic low-grade inflammation remain elusive.
Objectives:
We aimed to investigate how platelet activation and platelet-leukocyte interaction contribute to inflammation in obesity.
Methods:
We evaluated 87 patients with obesity (body mass index >30 kg/m2) in an observational cross-sectional study and investigated mechanisms of thromboinflammatory amplification using coculture models.
Results:
We demonstrated increased platelet activation and platelet-monocyte aggregate formation during obesity, which was associated with CD16 and tissue factor (TF) expression on monocytes. Platelet and monocyte activation were associated with metabolic syndrome and markers of increased high cardiovascular risk in obesity. Functional experiments with isolated cells highlighted platelet orchestration of monocyte functions leading to TF expression and proinflammatory mediator secretion. Platelet-monocyte interaction ex vivo reciprocally activated monocytes and platelets, inducing mediator secretion from both cells. Increased TF, CD16, and mediator secretion by monocytes and platelets occurred partially through CD62P-, CD40L-, and integrin αIIb β3-dependent signaling. Finally, conditioned medium from platelet-monocyte cocultures promoted endothelial cell activation through the interleukin 1 receptor.
Conclusion:
Our data reveal mechanisms involving a reciprocal platelet-monocyte activation amplification loop that was associated with cardiometabolic risk and supports thromboinflammation in obesity.
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