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Purpose: Activin A (AT-A), a member of the TGF-β superfamily is produced by numerous cell types physiologically regulating repair. Increases in AT-A is seen with tissue damage-if de-regulated a pro-inflammatory response ensues. Emerging evidence implicates activin-related inflammation and fibrosis in lung allograft reperfusion injury. Follistatin (FST), the endogenous antagonist of AT-A, mitigates its pro-inflammatory actions. We hypothesise that an elevated AT-A/FST ratio may contribute to the pro-inflammatory milieu typically seen in the early post-lung transplant (LTx) period. If so, this may be amenable to therapeutic manipulation through administration of exogenous FST. Methods: Serum for consecutive patients undergoing LTx from Feb 2014 were collected at 2, 6, 12 and 24 weeks post-LTx. Levels of AT-A, B and FST were measured by Elisa and specific radio-immunoassays, and compared to normals. Clinical events prospectively recorded included PGD, acute rejection, infection, lung function and hospital admissions. Data was analysed using paired and un-paired T-tests. Results: The study cohort consisted of 48 LTx patients (mean age 55.4, male n= 29, BSLTx n= 47). Indications for LTx included COPD (n= 24), ILD (n= 11), CF (n= 7) and misc (n = 6). Incremental decreases in AT-A were seen from a peak at 2 weeks to 12 weeks (p< 0.05). In contrast serum FST was unchanged between 2 and 12 weeks with a late significant increase between 12 and 24 weeks (p< 0.01). Comparing to normative data, serum AT-A remains elevated in LTx recipients at 24 weeks (p< 0.01); FST remains significantly lower. When comparing P/F ratios < 300 and > 300 at 24 hours, a difference in mean (p< 0.01) FST and mean AT-A to FST ratio (p= 0.01) was observed. Those with stable vs unstable clinical courses, defined as readmissions for rejection or infection, did not differ in their AT-A or FST concentrations. Older age was observed with higher mean AT-A (p= 0.02). Conclusion: Whilst, AT-A remains significantly elevated 6 months after lung transplantation, a 12 week lag is seen before FST increases. Further work is required to evaluate whether the pro-inflammatory environment due to unopposed early action of AT-A may contribute to the pathogenesis of CLAD. If so, FST may represent a therapeutic option to minimise inflammation in the early post-transplant period.