Abstract Rationale Pulmonary embolism (PE) after double lung transplantation (DLT) complicates between 4-15% of DLT cases. It is yet unclear what role early infections, the ensuing inflammation, or other mechanisms of inflammation have in the development of PE after DLT. The microbiomic signatures of patients after DLT with PE have yet to be investigated. It is well known that inflammation, whether from infection or other causes, increases the risk of PE. Meanwhile, the post transplant period for lung recipients is a time fraught with increased risk of both inflammation and infection. Differentiating the microbiome signature of patients with PE after DLT can aid in hypothesis generation for future exploration of causal links. Methods We performed a cross sectional analysis of 16S RNA gene sequencing as well as profiled the host immune response from bronchial alveolar lavage (BAL) samples obtained from 112 DLT recipients at a quaternary center. Comparisons were made between patients who developed PE and those who did not. Results Of 112 DLT recipients, 31 patients experienced PE and 81 did not. Age, gender, BMI, and race were similar pre-transplant between these two groups. Pulmonary function testing and right heart catheter values were also similar, as was indication for transplant. Ischemic time, need for transfusions intraoperatively, ICU days post operatively, and time to extubation also did not differ between the groups. GMCSF levels were higher in the no PE cohort (p = 0.022) and IP10 and MIG levels were higher in the PE cohort (p = 0.02, p = 0.023). There were significant differences in bacteria identified. The Serratia genus was represented much more often in the PE cohort whereas Fusobacterium and Achromobacter species were more prevalent in the no PE cohort. Conclusion Patients undergoing DLT who experienced PE were more likely to have indicators of upregulated T-cell signaling compared to their no PE counterparts which showed increased neutrophil signaling. The differences in the microbiome included more prevalent Serratia species in the PE cohort and Fusobacterium and Achromobacter species in the no PE group. It is possible differences in the microbiomes of these patients and ensuing cytokine signaling may affect the risk for pulmonary embolism and should be a target for further studies. This abstract is funded by: None
Slagle et al. (Fri,) studied this question.