Abstract
| Original language | English |
|---|---|
| Article number | e140948 |
| Number of pages | 16 |
| Journal | PLoS ONE |
| Volume | 11 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2016 |
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Substantial Increases Occur in Serum Activins and Follistatin during Lung Transplantation. / de Kretser, David M; Bensley, Jonathan G; Phillips, David James; Levvey, Bronwyn; Snell, Gregory I; Lin, Enjarn; Hedger, Mark P; O'Hehir, Robyn E.
In: PLoS ONE, Vol. 11, No. 1, e140948, 2016.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Substantial Increases Occur in Serum Activins and Follistatin during Lung Transplantation
AU - de Kretser, David M
AU - Bensley, Jonathan G
AU - Phillips, David James
AU - Levvey, Bronwyn
AU - Snell, Gregory I
AU - Lin, Enjarn
AU - Hedger, Mark P
AU - O'Hehir, Robyn E
PY - 2016
Y1 - 2016
N2 - BACKGROUND: Lung transplantation exposes the donated lung to a period of anoxia. Re-establishing the circulation after ischemia stimulates inflammation causing organ damage. Since our published data established that activin A is a key pro-inflammatory cytokine, we assessed the roles of activin A and B, and their binding protein, follistatin, in patients undergoing lung transplantation. METHODS: Sera from 46 patients participating in a published study of remote ischemia conditioning in lung transplantation were used. Serum activin A and B, follistatin and 11 other cytokines were measured in samples taken immediately after anaesthesia induction, after remote ischemia conditioning or sham treatment undertaken just prior to allograft reperfusion and during the subsequent 24 hours. RESULTS: Substantial increases in serum activin A, B and follistatin occurred after the baseline sample, taken before anaesthesia induction and peaked immediately after the remote ischemia conditioning/sham treatment. The levels remained elevated 15 minutes after lung transplantation declining thereafter reaching baseline 2 hours post-transplant. Activin B and follistatin concentrations were lower in patients receiving remote ischemia conditioning compared to sham treated patients but the magnitude of the decrease did not correlate with early transplant outcomes. CONCLUSIONS: We propose that the increases in the serum activin A, B and follistatin result from a combination of factors; the acute phase response, the reperfusion response and the use of heparin-based anti-coagulants.
AB - BACKGROUND: Lung transplantation exposes the donated lung to a period of anoxia. Re-establishing the circulation after ischemia stimulates inflammation causing organ damage. Since our published data established that activin A is a key pro-inflammatory cytokine, we assessed the roles of activin A and B, and their binding protein, follistatin, in patients undergoing lung transplantation. METHODS: Sera from 46 patients participating in a published study of remote ischemia conditioning in lung transplantation were used. Serum activin A and B, follistatin and 11 other cytokines were measured in samples taken immediately after anaesthesia induction, after remote ischemia conditioning or sham treatment undertaken just prior to allograft reperfusion and during the subsequent 24 hours. RESULTS: Substantial increases in serum activin A, B and follistatin occurred after the baseline sample, taken before anaesthesia induction and peaked immediately after the remote ischemia conditioning/sham treatment. The levels remained elevated 15 minutes after lung transplantation declining thereafter reaching baseline 2 hours post-transplant. Activin B and follistatin concentrations were lower in patients receiving remote ischemia conditioning compared to sham treated patients but the magnitude of the decrease did not correlate with early transplant outcomes. CONCLUSIONS: We propose that the increases in the serum activin A, B and follistatin result from a combination of factors; the acute phase response, the reperfusion response and the use of heparin-based anti-coagulants.
UR - http://www.ncbi.nlm.nih.gov/pubmed/26820896
U2 - 10.1371/journal.pone.0140948
DO - 10.1371/journal.pone.0140948
M3 - Article
VL - 11
JO - PLoS ONE
JF - PLoS ONE
SN - 1932-6203
IS - 1
M1 - e140948
ER -