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Increased M1 Macrophages Infiltration Is Associated with Thrombogenesis in Rheumatic Mitral Stenosis Patients with

Guixin He1,2, Wei Tan2, Bingjian Wang3

  • 1Department of Cardiology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.

Plos One
|March 2, 2016
PubMed

Insights

Proinflammatory M1 macrophages and NLRP3 inflammasomes are linked to atrial fibrillation (AF) and thrombus formation in rheumatic mitral stenosis patients. This suggests a role in progressive atrial inflammation and thrombogenesis.

Area of Science:

  • Cardiology
  • Immunology
  • Pathology

Background:

  • Atrial fibrillation (AF) is a common arrhythmia, but the role of macrophage subsets in AF-related thrombogenesis remains unclear.
  • Understanding these mechanisms is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of M1 and M2 macrophages and associated cytokines in the thrombogenesis of patients with rheumatic mitral stenosis (MS) and AF.
  • To explore the relationship between macrophage infiltration, inflammasome activation, and cardiomyocyte apoptosis in MS-related AF with thrombosis.

Main Methods:

  • Analysis of 71 left atrial appendage specimens from MS patients with or without thrombosis.
  • Immunohistochemistry to detect M1/M2 macrophage infiltration.
  • Western blot and TUNEL assay to assess inflammasome components, IL-1β expression, and cardiomyocyte apoptosis.

Main Results:

  • Proinflammatory M1 macrophages were predominant in MS patients with AF and thrombus.
  • NLRP3 inflammasomes and IL-1β were activated in these patients.
  • Increased cardiomyocyte apoptosis correlated with thrombogenesis.

Conclusions:

  • M1 macrophage infiltration and NLRP3 inflammasome over-activation may contribute to atrial inflammation and thrombogenesis in MS patients with AF.
  • These findings highlight potential therapeutic targets for managing AF-related thrombosis.

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