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Tying up PGE2 with albumin to relieve immunosuppression in cirrhosis

The function of the innate immune system is suppressed in patients with acutely decompensated cirrhosis and predisposes these patients to bacterial infections. A new study shows that increased synthesis of the immunosuppressive prostaglandin PGE2 by circulating monocytes and resident macrophages and impaired hepatic synthesis of human serum albumin (HSA) are major contributors to immune suppression in cirrhosis (pages 518–523). The authors' data suggests a new avenue for therapy in acute decompensation of cirrhosis.

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Figure 1: Cirrhosis-associated immune suppression may be mediated by PGE2 and treated with albumin administration.

Kim Caesar/Nature Publishing Group

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Correspondence to Vicente Arroyo.

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V.A. has a grant from Grifols.

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Arroyo, V., Moreau, R. Tying up PGE2 with albumin to relieve immunosuppression in cirrhosis. Nat Med 20, 467–469 (2014). https://doi.org/10.1038/nm.3553

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