Siobhan Crittenden

ORIGINAL ARTICLE Marie Goepp, Centre for Inflammation Research, Queen’s Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ UK These authors have contributed equally to this work and share first authorship Search for more papers by this author Siobhan Crittenden, Centre for Inflammation Research, Queen’s Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ UK These authors have contributed equally to this work and share first authorship Search...

Abstract The gut microbiota fundamentally regulates intestinal homeostasis and disease partially through mechanisms that involve modulation of regulatory T cells (Tregs), yet how the microbiota-Treg cross-talk is physiologically controlled is incompletely defined. Here, we report that prostaglandin E2 (PGE2), a well-known mediator of inflammation, inhibits mucosal Tregs in a manner depending on the gut microbiota. PGE2 through its receptor EP4 diminishes Treg-favorable commensal microbiota.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a life-threatening neutrophil-dominant disease with a significant morbidity and mortality for which effective therapies are currently lacking.1 Excessive pulmonary neutrophil recruitment mediates lung tissue damage, despite the beneficial role of neutrophils in promoting tissue repair.2 Therefore, there is a need for more effective medicinal agents for use in these severe and often lethal lung injury syndromes.1 Interleukin...