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Intro Parapneumonic effusions complicate up to 40% of pneumonia hospitalisations and are associated with 3–6 fold increase in mortality. Progressive fibrinous septations increase the complexity of the parapneumonic effusion and render drainage more difficult. Macrophages are the dominant immune cells in the healthy pleural space, however, their role in parapneumonic effusions remains poorly understood.Methods Patients in St James’s Hospital undergoing drainage of parapneumonic effusion or drainage of transudative effusion (fluid accumulation secondary to hydrostatic pressure) were recruited, and clinical data recorded. Peripheral blood mononuclear cells (PBMCs) from healthy donors were differentiated into macrophages and incubated with the acellular component of pleural fluid for 24 hours to mimic the pleural effusion environment. Macrophage phenotype was interrogated by flow cytometry, and macrophage thrombin generation was evaluated using a fluorogenic assay.Results 10 parapneumonic and 8 transudative effusions patients were recruited. Pleural fluid skewed macrophages toward an M2 phenotype, with increased expression of CD163 (p=0.021) and reduced expression of CD40 (p=0.009). Transudative fluid upregulated CD163 more than parapneumonic fluid (p=0.045). (figure 1a) Functionally, pleural fluid enhanced macrophage-dependent thrombin generation, reducing lagtime (p<0.0001), increasing peak thrombin (p=0.0175), and increasing endogenous thrombin potential (ETP) (p<0.0001), in a dose-dependent manner. Parapneumonic fluid promoted greater induction of macrophage-dependent thrombin generation than transudative fluid (figure 1b).Conclusion These findings confirm that pleural fluid influences macrophage phenotype and increases their thrombogenic potential. This highlights the macrophage as a key player in the fibrin deposition characteristic of complicated parapneumonic effusions and suggests a potential immunothrombotic target for patients with pleural infection.